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KEY TOPICS IN OTOLARYNGOLOGY AND HEAD AND NECK SURGERY
SECOND EDITION

The KEY TOPICS Series
Advisors: T.M.Craft Department of Anaesthesia and Intensive Care, Royal United Hospital, Bath, UK C.S.Garrard Intensive therapy Unit, John Radcliffe Hospital, Oxford, UK P.M.Upton Department of Anaesthesia,Royal Cornwall Hospital, Treliske, Truro, UK
Obstetrics and Gynaecology, Second Edition Accident and Emergency Medicine Paediatrics, Second Edition Orthopaedic Surgery Ophthalmology Psychiatry General Surgery Renal Medicine Trauma Chronic Pain Oral and Maxillofacial Surgery Oncology Cardiovascular Medicine Neurology Neonatology Gastroenterology Thoracic Surgery Respiratory Medicine Orthopaedic Trauma Surgery Critical Care Otolaryngology, Second Edition Forthcoming titles include: Anaesthesia, Third Edition Accident and Emergency Medicine, Second Edition Urology Ophthalmology, Second Edition Acute Poisoning

KEY TOPICS IN OTOLARYNGOLOGY and Head and Neck Surgery
Second Edition

N.J.ROLAND MD, FRCS Consultant in Otolaryngology and Head and Neck Surgery, Honorary Lecturer, Liverpool University, University Hospital Aintree, Liverpool, UK R.D.R.McRAE FRCS Consultant in Otolaryngology and Head and Neck Surgery, Colchester General Hospital, Colchester, Essex, UK A.W.McCOMBE MD, FRCS Consultant in Otolaryngology and Head and Neck Surgery, Frimley Park Hospital, Surrey, UK

© BIOS Scientific Publishers Limited, 2001 First published 1995 Second Edition 2001 This edition published in the Taylor & Francis e-Library, 2005. “To purchase your own copy of this or any of Taylor & Francis or Routledge’s collection of thousands of eBooks please go to www.eBookstore.tandf.co.uk.” All rights reserved. No part of this book may be reproduced or transmitted, in any form or by any means, without permission. A CIP catalogue record for this book is available from the British Library. ISBN 0-203-45041-8 Master e-book ISBN

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CONTENTS

Acoustic neuroma Acute suppurative otitis media Adenoids Allergic rhinitis Anaesthesia—general Anaesthesia—local Benign neck lumps Caloric tests Cervical lymphadenopathy Choanal atresia Cholesteatoma Chronic suppurative otitis media Chronic suppurative otitis media—complications Clinical assessment of hearing Clinical governance and audit Cochlear implants Congenital hearing disorders Cosmetic surgery Day case ENT surgery Epiglottitis Epistaxis Evidence based medicine Evoked response audiometry Examination of the ear Examination of the nose

1 4 7 10 13 18 22 26 28 32 34 37 41 44 48 52 58 62 66 69 72 75 78 82 85

vi

Examination of the throat External ear conditions Facial nerve palsy Facial pain and headache Foreign bodies Functional endoscopic sinus surgery Globus pharyngeus Halitosis Hearing aids HIV infection Hypopharyngeal carcinoma Impedance audiometry Intrinsic rhinitis Labyrinthitis Laryngeal carcinoma Laryngectomy Lasers in ENT Literature evaluation Mastoidectomy Medico-legal aspects of ENT surgery Menière’s disease Nasal granulomata Nasal polyps Nasal trauma Nasopharyngeal tumours Neck dissection Neck space infection Noise-induced hearing loss Non-organic hearing loss Oral cavity carcinoma

88 91 94 99 104 109 114 116 118 122 125 129 132 135 139 144 148 152 159 162 167 170 174 177 180 185 188 192 195 197

vii Oroantral fistula Oropharyngeal carcinoma Otalgia Otitis externa Otitis media with effusion (glue ear) Otoacoustic emissions Otological aspects of head injury Otorrhoea Otosclerosis Ototoxicity Paediatric airway problems Paediatric endoscopy Paediatric hearing assessment Papilloma of the larynx Perilymph fistula Pharyngeal pouch Pharyngocutaneous fistula Presbyacusis Pure tone audiogram Radiology in ENT Radiotherapy Reconstructive surgery Salivary gland diseases Salivary gland neoplasms Septal perforation Sinonasal tumours Sinusitis Sinusitis—complications Smell and taste disorders Snoring and obstructive sleep apnoea 201 203 207 210 214 217 219 222 224 229 233 237 239 242 245 247 250 253 256 259 265 268 272 275 278 280 285 291 294 297 .

viii Speech audiometry Speech therapy in head and neck surgery Speech therapy in non-malignant voice disorders Stridor and stertor Sudden hearing loss Thyroid disease—benign Thyroid disease—malignant Tinnitus Tonsil diseases Tonsillectomy Tracheostomy Tympanoplasty Tympanosclerosis Vertigo Vestibular function tests Vocal cord palsy Index 301 304 308 311 315 317 323 328 331 334 337 341 343 345 348 352 355 .

CONTRIBUTORS P. UK Austin Leach Consultant Anaesthetist.Ramadan Consultant ENT Surgeon.Charters Consultant Anaesthetist. Liverpool. Colchester General Hospital.Saeed Consultant Otolaryngologist. Manchester Royal Infirmary. Royal Liverpool University Hospital. Liverpool. Liverpool.F.Bradley Consultant Otolaryngologist. UK P. UK T. UK Huw Lewis-Jones Consultant Radiologist. Clatterbridge Centre for Oncology. Liverpool. Queen Elizabeth Medical Centre. University Hospital Aintree.H. Liverpool. UK J. UK Michael Pringle Consultant Otolaryngologist. Queens Medical Centre. Wirral.R.Watkinson Consultant Head and Neck and Thyroid Surgeon. Queen Alexandra Hospital. University Hospital Aintree.Niranjan Consultant Plastic and Reconstructive Surgeon. Glasgow Royal Infirmary.J. UK PamYoung Senior Speech and Language Therapist. Glasgow. UK S. Portsmouth. UK M. Queen Elizabeth Hospital. University Hospital Aintree. UK George Browning Professor of Otolaryngology. Bebington. UK A. UK . University Hospital Aintree. Nottingham. Essex.Lesser Consultant ENT Surgeon.S. Birmingham. Manchester. Colchester.C. Royal Liverpool University Hospital. Liverpool. UK N.Shenoy Consultant Oncologist.

warm-same central processing unit contralateral routing of signal cerebro-spinal fluid chronic suppurative otitis media computerized tomography delayed speech feedback digital signal processing external auditory meatus Epstein-Barr virus electrocochleography extra-capsular spread . hydroxydaunorubicin. oncovine (vincristine) and prednisolone Creutzfeldt Jakob disease cold-opposite. genital anomalies. heart disease.ABBREVIATIONS AA AJC ANCA ASA ASOM BAHA BDNF BERA BEHA BIPP BW c-ANCA CHARGE CHI CHOP CJD COWS CPU CROS CSF CSOM CT DSF DSP EAM EBV ECochG ECS androgenic alopecia American Joint Committee anti-neutrophil cytoplasmic antibody American Society of Anesthesiologists Acute suppurative otitis media bone-anchored hearing aid brain-derived neurotrophic factor brainstem evoked response audiometry behind the ear hearing aid bismuth iodoform paraffin paste body-worn hearing aid cytoplasmic anti-neutrophil cytoplasmic antibody colobama. ear abnormalities and deafness Commission for Health Improvement cyclophosphamide. atresia choanae. retarded growth and development.

age. stage and histology glial cell line-derived neurotrophic factor glossopharyngeal neuralgia Haemophilus influenzae type B hearing level holmium: YAG (laser) half-peak level half-peak level elevation human papillomavirus herpes simplex virus internal auditory meatus inner hair cell intrinsic rhinitis ‘in the canal’ ‘in the ear’ potassium titanyl phosphate (laser) multiple endocrine neoplasia magnetic resonance imaging minor salivary gland carcinoma nucleoside analogue National Confidential Enquiry into Perioperative Deaths neodymium doped-yttrium aluminium garnet (laser) neurofibromatosis type 2 non-Hodgkin’s lymphoma National Institute for Clinical Excellence noise-induced hearing loss non-nucleoside .xi EEMG EMLA EPS Er:YAG ESR EUA FBC FESS FNA FNAC FTA GASH GDNF GPN HIB HL Ho:YAG HPL HPLE HPV HSV IAM IHC IR ITC ITE KTP MEN MRI MSGC NARTI NCEPOD Nd-YAG NF2 NHL NICE NIHL NNRTI evoked electromyogram eutectic mixture of local anaesthetic exophthalmos producing substance erbium: YAG (laser) erythrocyte sedimentation rate examination under anaesthetic full blood count functional endoscopic sinus surgery fine needle aspiration fine needle aspiration cytology fluorescent treponemal antibody test gender.

cyclophosphamide and bleomycin vanillylmandelic acid . prednisolone.xii NOHL NPC OAE ODS OHC p-ANCA PCT PE PI PHN PLF PORP PRIST pTNM PTS RAST SCC SCPL SMAS SMR SNHL SRT STIR SVR TENS TEOAE TGN TMJ TORP TPHA TSH TTS UICC URTI USS VAPEL-B VMA non-organic hearing loss nasopharyngeal carcinoma otoacoustic emission optimum discrimination score outer hair cell perinuclear anti-neutrophil cytoplasmic antibody percutaneous tracheostomy pharyngo-oesophageal protease inhibitors postherpetic neuralgia perilymph fistula partial ossicular replacement prosthesis plasma radioimmunosorbent test pathological staging permanent threshold shift radioallergosorbent test squamous cell carcinoma supracricoid partial laryngectomy superficial muscle and aponeurotic system submucosal resection sensorineural hearing loss speech reception threshold short tau inversion recovery surgical voice restoration transcutaneous electrical nerve stimulation transient evoked otoacoustic emission trigeminal neuralgia temperomandibular joint total ossicular replacement prosthesis treponema pallidum haemagglutination test thyroid stimulating hormone temporary threshold shift International Union Against Cancer upper respiratory tract infection ultrasound scan vincristine. etoposide. adreomycin.

xiii WG WHO WNG Wegener’s granulomatosis World Health Organization White Noise Generators .

British Approved Name). BAN.rlNN to appear exclusively Former BAN amoxycillin amphetamine amylobarbitone amylobarbitone sodium beclomethasone benorylate busulphan butobarbitone carticaine cephalexin cephamandole nafate cephazolin cephradine chloral betaine chlorbutol chlormethiazole chlorathalidone cholecalciferol cholestyramine clomiphene colistin sulphomethate sodium corticotrophin cysteamine danthron rINN/new BAN amoxicillin amfetamine amobarbital amobarbital sodium beclometasone benorilate busulfan butobarbital articane cefalexin cefamandole nafate cefazolin cefradine cloral betaine chlorobutanol clomethiazole chlortalidone colecalciferol colestyramine clomifene colistimethate sodium corticotropin mercaptamine dantron rlNN epinephrine tetracaine bendroflumethiazide trihexyphenidyl chlorphenamine dicycloverine dosulepin formoterol fludroxycortide furosemide hydroxycarbamide lidocaine levomepromazine methylthoninium mitoxantrone chlormethine acenocoumarol norepinephrine pentoxyifylline procaine benzylpenicillin calcitonin (salmon) moxisylyte levothyroxine sodium alimemazine amethocaine bendrofluazide benzhexol chlorpheniramine dicyclomine dothiepin eformoterole flurandrenolone frusemide hydroxyurea lignocaine methotrimeprazine methylene blue mitozantrone mustine nicoumalone 2noradrenaline oxypentifylline procaine penicillin salcatonin thymoxamine thyroxine sodium trimeprazine .NAMES OF MEDICAL SUBSTANCES In accordance with directive 92/27/EEC. List 1 . Recommended International Non-proprietary Name. this book adheres to the following guidelines on naming of medicinal substances (rINN.Both names to appear UK Name 2adrenaline List 2 .

xv desoxymethasone dexamphetamine dibromopropamidine dienoestrol dimethicone(s) dimethyl sulphoxide doxycycline hydrochloride (hemihydrate hemiethanolate) ethancrynic acid ethamsylate ethinyloestradiol ethynodiol flumethasone flupenthixol gestronol guaiphenesin hexachlorophane hexamine hippurate hydrosyprogesterone hexanoate indomethacin lysuride methyl cysteine methylphenobarbitone oestradiol oestriol oestrone oxethazaine pentaerythritol tetranitrate phenobarbitone pipothiazine polyhexanide potassium cloazepate pramoxine prothionamide quinalbarbitone riboflavine sodium calciumedetate sodium cromoglycate desoximetasone dexamfetamine dibrompropamidine dienestrol dimeticone dimethyl sulfoxide doxycycline hyclate etacrynic acid etamsylate ethinylestradiol etynodiol flumetasone flupentixol gestonorone guaifenesin hexachlorophene methenamine hippurate hydroxyprogesterone caproate indometacin lisuride mecysteine methylphenobarbital estradiol estriol estrone oxetacaine pentaerithrityl tetranitrate phenobarbital pipotiazine polihexanide dipotassium clorazepate pramocaine protionamide secobarbital riboflavin sodium calcium edetate sodium cromoglicate sodium ironedetate sodium picosulphate sorbitan monostearate stilboestrol sulphacetamide sulphadiazine sulphadimidine sulphaguanadine sulphamethoxazole sulphasalazine sulphathiazole sulphinpyrazone tetracosactrin thiabendazole thioguanine thiopentone urofollitrophin sodium feredetate sodium picosulfate sorbitan stearate diethylstilbestrol sulfacetamide sulfadiazine sulfadimidine sulfaguanadine sulfamethoxazole sulfasalazine sulfathiazole sulfinpyrazone tetracosactide tiabendazole tioguanine thiopental urofollitropin .

Pathology The medial portions of the cranial nerves are covered with glial stroma. numbness and paraesthesiae may all occur. The sexes are equally affected and. They arise from Schwann (neurolemmal) cells. Some patients have normal hearing (5%). 3. 4. The majority of these tumours are unilateral. 1. two phases can be recognized: an otological phase in which a small tumour compresses structures in the meatus.ACOUSTIC NEUROMA Acoustic neuroma represents 8% of all intracranial tumours and 80% of cerebellopontine angle tumours. The annual incidence is approximately 1 in 100 000. Facial pain. The commonest nerve of origin is the superior vestibular nerve. rarely. Histologically the tumour consists of packed sheaves of connective tissue cells (fasciculated) or may be composed of a disorderly loose network of cells with intercellular vacuoles and cysts (reticular pattern). Clinical features Clinically. Like most motor nerves. Ataxia and unsteadiness develop with . Vertigo is an unusual complaint as compensation for vestibular nerve damage usually keeps pace with the slow rate of neural destruction. and the small proportion that are bilateral (5%) are seen in multiple neurofibromatosis type 2 (NF2). leading to a sudden increase in size and therefore marked symptoms such as acute vertigo or sudden deafness. Discomfort and dull aching around the ear and mastoid area are probably caused by posterior fossa dura irritation due to the enlarging tumour. Many surgeons prefer therefore the term vestibular schwannoma to acoustic neuroma. This is an autosomal dominant disease due to an aberration on the long arm of chromosome 22. the cochlear nerve. Headache. and a neurological phase as the tumour expands medially into the cerebellopontine angle. 2. Haemorrhage can occur (particularly in the reticular type). Gradual and progressive unilateral deafness is the usual presenting symptom (90%). Late symptoms. whatever the time of onset and rate of progression. Sudden onset hearing loss can occur (10%). The deafness is often associated with tinnitus (70%). which for the vestibular nerve is usually within the internal auditory meatus. Trigeminal nerve symptoms. the presentation is most often between the ages of 40 and 60. followed by the inferior vestibular and then. Otological symptoms. the facial nerve is resistant to pressure deformity and symptoms of facial weakness or hemifacial spasm are uncommon. Acoustic neuromas originate at the junction of the glial and Schwann cells. Macroscopically the tumour appears as a firm yellowish encapsulated mass with the nerve splayed out on its surface.

Diplopia due to pressure on the VIth cranial nerve. used for the diagnosis of an acoustic neuroma. Terminal symptoms. and this gives a low-false negative rate of around 5%. Congenital cholesteatoma. This is therefore the investigation of choice and is used for screening. Cholesterol granuloma of the petrous apex. this ideal is not always possible. Loss of the corneal reflex is an early sign of trigeminal nerve impairment. 3. It demonstrates a retrocochlear lesion by an increased latency between N1 and N5 waves. 2. 5. Facial nerve impairment is usually of the sensory element and can be elicited as a lack of taste on electrogustometry or loss of lacrimation on Schirmer’s test. with preservation of all neural function and with minimal morbidity and mortality. general examination will usually reveal no abnormalities. Computerized tomography (CT) scanning with high definition and enhancement techniques will accurately diagnose and delineate most tumours. Stapedial reflex decay can be measured using impedance audiometry. The raised CSF pressure causes failing vision due to papilloedema. 6. Investigations 1. and hoarseness with dysphagia due to involvement of the IXth and Xth nerves is rare. Nystagmus when present may be of the vestibular or cerebellar type. The patient may have a unilateral neural hearing loss. but should only be used when MRI is unavailable. If the pure tone threshold hearing loss is greater than 70 dB. Aneurysm of the basilar or vertebral arteries. Vestibular investigations. Special audiometric and vestibular testing are now rarely. Neuroma of the VIIth nerve. The most accurate means of identifying small intracanalicular tumours is magnetic resonance imaging (MRI) with gadolinium enhancement. if ever. but there is no abnormality in some patients with small tumours. 3. 4. headache. 5. the accuracy of audiometric testing is poor. A unilateral or asymmetrical sensorineural hearing loss can usually be demonstrated by a pure tone audiogram. 7. Acoustic neuromas (constitute 80% of cerebellopontine angle tumours). Neurological signs of the other cranial nerve palsies will eventually become apparent. 2. Radiological investigations. abnormally rapid adaptation and disproportionately poor speech discrimination. Caloric responses are usually reduced in or absent from the affected side. Management The ideal management is a single stage total removal of the lesion. Differential diagnosis of a tumour at the cerebellopontine angle 1. Cerebellar tumour. Meningioma.2 OTOLARYNGOLOGY progressive brain stem displacement and cerebellar involvement. However. alteration in conscious level and eventually coma. Audiometry. Later the patient may have evidence of ataxia. Each case must be . Slight facial weakness may show as a delay in the blink reflex. Hypaesthesia of the posterior external ear canal on the side of the hearing loss should raise the index of suspicion (Hitselberger sign). The hearing loss is classically a neural lesion with no loudness recruitment. Brainstem electric response audiometry has only a 3% false-negative rate. In the otological phase.

Radiology in ENT. 257. Acta Neurochir 1997. 2. Conservative management Small. 1. Translabyrinthine approach. Vertigo. Syms C. 2. p. p. Cerebrospinal fluid leak (often down the Eustachian tube) and meningitis are also relatively common. slow-growing tumours in elderly patients can be watched by carrying out CT or MRI scanning at regular intervals to gauge the rate of expansion. In: Ludman H. There are three surgical approaches to the cerebellopontine angle and the choice depends on the position and size of the tumour and preoperative assessment by the otoneurologist and neurosurgeon. Kveton JF. 6th edn. Stereotactic radiosurgery (gamma knife) has been applied to the tumour margin to control growth. Retrosigmoid approach. so this approach is also used for tumours when there is good hearing. 346. 1993. 1998. This route is feasible when there is CSF between the lateral margin of the tumour and the lateral margin of the IAM (cochlea). The patient’s hearing and facial nerve can be preserved. The main disadvantage is that there is a 15% risk of the patient developing epilepsy. Tumours of the auditory-vestibular nerve. In the UK. 335–343. Wilson J (ed). Vestibular function tests.ACOUSTIC NEUROMA 3 assessed on its own merits. Annual MRI scans show that around 60% of acoustic neuromas are not growing. London: Arnold. Hyperfractionated stereotactic radiotherapy is considered by some to be the primary treatment modality of choice. Costs and effects of microsurgery versus radiosurgery in treating acoustic neuroma. The facial nerve can be preserved but all hearing is lost. site and rate of growth of the lesion. The morbidity and mortality from both tumour growth and its operative removal increase with large tumours. 2000. driving is banned for 1 year following this procedure. Head and Neck Surgeons. 1:53–63. Current Opinion in Otolaryngology and Head and Neck Surgery. Related topics of interest Evoked response audiometry. Early diagnosis and removal of these tumours should therefore be the rule. 350. 3. This gives a limited access and is usually used for small intrameatal tumours. Removal of acoustic neuroma is associated most commonly with injury to the VIIth and VIIIth cranial nerves. p. . p. British Association of Otolaryngologists. Further reading Chandler CL. These are popular treatments with patient self-help groups and are increasingly advocated in the USA. 3. Acoustic schwannoma. Opponents to this view argue that future microsurgery may be more difficult and there is a theoretical risk of inducing malignant change. but an extended middle fossa approach can be used for larger ones. A small tumour can be extracted from the meatus with negligible hazard and preservation of the facial nerve. 139:942–945. 327. 78. 1. Radiosurgery or radiotherapy. Middle fossa route. Evaluation and management of acoustic neuroma. Effective Head and Neck Cancer Management. Microsurgery. Brackmann D. Van Roijen L. Wright T (eds) Diseases of the Ear. 49(5): 3–16. The approach tends to be used for patients with a severe sensorineural hearing loss (less than 70% speech discrimination). Hearing and the facial nerve can be preserved. 1993. British Journal of Hospital Medicine. This is the most common approach. 535–547. p. Second Consensus. Ramsden RT. with careful consideration of the age and general condition of the patient and the size. Tinnitus.

wide more horizontally placed eustachian tube. chest disease and eustachian tube dysfunction. Acute suppurative otitis media (ASOM) Aetiology This is a bacterial disease caused by pus forming organisms. Poor sanitation and hygiene. Classification It may be classified as acute or chronic with the suffix suppurative or nonsuppurative. with or without suppuration and a fourth category namely ‘adhesive otitis media’ has been used to describe tympanosclerosis (hyaline degeneration and calcification) and adhesion formation within the tympanic cavity but should more accurately be regarded as a sequelae of otitis media. direct extension from a bacterial or secondary to a viral upper respiratory tract infection being the most common aetiological factor. attic. Risk factors in all age groups are recurrent or chronic rhinosinusitis. the collective term for the eustachian tube. abnormal eustachian patency. Pathogenic bacteria have been isolated from the nasopharynx in up to 97% of children with ASOM. Haemophilus influenzae (30%) and Branhamella (Moraxella) catarrhalis (10%) being the most commonly implicated. Bacteria enter the middle-ear cleft via the eustachian tube. It may occur as a primary or a secondary infection after a viral acute non-suppurative otitis media. overcrowding and malnutrition are predisposing factors. tympanic cavity. cleft palate and submucous cleft palate.ACUTE SUPPURATIVE OTITIS MEDIA Definition Otitis media is an inflammation of part or all of the mucosa of the middle-ear cleft. aditus. a perforated tympanic membrane or more rarely be blood-borne. allowing contamination from the regurgitation of feed and when actively vomiting. Causes of the latter are nasopharyngeal tumours including adenoidal hypertrophy. antrum and mastoid air cells. ‘specific otitis media’ has been used to describe tuberculous and syphilitic otitis media as it may present acutely or chronically. A third category. . Infants have a short. Teething increases the incidence of infection. Children aged 3–7 years have the highest incidence. Streptococcus pneumoniae (40%). adenoiditis.

• Cerebellar. temporal lobe and perisinus abscess. Gradenigo’s syndrome. Conditions predisposing to ASOM should be treated on their own merit after resolution. for example coamoxiclav. Oral medication is adequate in the absence of complications. Pressure necrosis of this region may cause the drumhead to rupture allowing mucopus to drain into the external ear canal. In these circumstances. which may increase rapidly in intensity to become deep and throbbing. Systemic and topical decongestants have a theoretical adjuvant role. comprising signs of ASOM.e. Complications • Mucositis may progress to an osteomyelitis. • Citelli’s abscess (a subperiosteal abscess which has spread through the medial aspect of the mastoid. opposite to retraction). gleaned from bacterial sensitivity studies or lack of clinical response. 4. is a classic feature of petrositis. The drumhead takes on a full (i. Treatment 1. Children are usually fretful with a high pyrexia (> 39°C) and there may be signs of complications of ASOM. into the digastric fossa) or Bezold’s abscess (an abscess which has tracked inferiorly within the sheath of sternomastoid to form a fluctuant mass along its anterior border).ACUTE SUPPURATIVE OTITIS MEDIA 5 Clinical features The two main symptoms are: • Pain. angry appearance and pus may be seen bulging postero-inferiorly. namely acute mastoiditis. • Deafness. Rest in a warm. the latter occurring in about 14% of cases but resistance is increasing. The respective cranial nerves are only separated from the petrous apex by a layer of dura so that an extradural abscess or pachymeningitis (meningitis extending to the dural layer) of this region from a generalized meningitis may also cause the combined cranial nerve signs. well humidified room. if the mastoid air cells are affected and acute petrositis should the petrous apex become involved. an ipsilateral abducent nerve palsy causing paralysis of the external rectus and pain in the distribution of the ipsilateral trigeminal nerve. Deafness progresses as suppuration occurs and both symptoms may rapidly improve if rupture of the tympanic membrane produces a mucopurulent otorrhoea. they have not been proven to be of significant value. . • Extradural and subdural abscess. The initial event after infection is mucosal oedema causing Eustachian tube occlusion and a dull tympanic membrane on examination. 2. Hyperaemia rapidly follows and leashes of vessels may be seen running along or parallel to the malleus handle. initially described as a blocked ear and secondary to Eustachian tube dysfunction. Soon radial vessels are visible on the drumhead and a middle ear effusion occurs. 3. red. a -lactamase resistant antibiotic should be chosen. Antibiotics in an adequate dose administered until resolution. • Meningitis. Amoxicillin will cover the most common pathogens provided the patient is not allergic to penicillin and the organisms are not resistant.

Paediatric Infectious Diseases Journal. • High-tone sensorineural hearing loss. Cholesteatoma. 341. Further reading Haddad J Jr. Otolaryngologic Clinics of North America. p. ossicles and the medial wall of the middle ear. fixing the latter. 6:431–441. Sequelae of ASOM • Non-suppurative middle-ear effusion. Stutman HR. p. p. Related topics of interest Tympanoplasty. 13:27–34. Treatment of acute otitis media and its complications in pediatric otology.6 OTOLARYNGOLOGY • Lateral sinus thrombosis. Assessing the treatment alternatives for acute otitis media. • Erosion of the ossicular chain. 1992. p. Pichichero ME. . 1994. 38. The at-risk population (6%) are that group of patients with a congenital dehiscence of the horizontal portion of the facial nerve. perhaps secondary to bacterial toxins migrating across the round window. Chronic suppurative otitis media. especially following recurrent episodes of ASOM. • Otitic hydrocephalus. 35. Comparison of cefprozil with other antibiotic regimes in the treatment of children with acute otitis media. Clinical Infectious Diseases. These persist for over 30 days in 40% of children and for over 3 months in 10%. • Sequelae of ASOM complications. 42. 1994. in particular the long process of the incus. • Serous and suppurative labyrinthitis. • Adhesions between the tympanic membrane. 14 (suppl 2): 204–208. • Tympanic membrane perforation. Chronic suppurative otitis media—complications. • Tympanosclerosis which may spread from the tympanic membrane to the ossicular chain. rarely extending in an antegrade direction to thrombose the internal jugular vein and in a retrograde direction causing a cavernous sinus thrombosis. Arguedas AG. • Lower motor neurone facial nerve paralysis.

Pathology Inflammation due to acute viral and bacterial infections results in hyperplasia with enlargement and multiplication of the lymphoid follicles. The symptoms caused by hypertrophy result not from the actual size of the lymphoid mass. Clinical features 1. Nasal discharge and postnasal drip or catarrh may develop as a result of secondary chronic rhinitis and sinusitis. a short upper lip. Nasal obstruction leads to mouth breathing. but from the relative disproportion in size between the adenoids and the cavity of the nasopharynx. The child with the ‘classic’ adenoid facies appearance (an open lip posture. The clinical features of adenoid hypertrophy are not always clear cut. but in many children it is impossible to assess the adenoids in this way. They are a normal structure with a function in the production of antibodies (IgA. some children may suffer from episodes of sleep apnoea. Most of the pathological effects related to the adenoids are due to this increase in size. The most useful investigation is a lateral softtissue radiograph. Infants may have difficulty in feeding because they have to stop sucking intermittently to take a breath. but in general they attain their maximum size between the ages of 3 and 8 years and then regress. prominent upper incisors. snoring and hyponasal speech. Symptoms are frequently wrongly attributed to enlarged adenoids. 2. Fibreoptic endoscopy is useful if tolerated by the child. The effect of the enlargement is to produce obstruction of the nasal airways and possibly obstruction of the Eustachian tubes. IgG and IgM). Eustachian tube obstruction may result in earache and deafness due to recurrent bouts of acute otitis media and otitis media with effusion (glue ear). a thin nose and a hypoplastic maxilla with a high arched palate) is rarely seen. This will give a measure of the absolute size of the adenoids and an assessment of their . In some children examination of the nasopharynx with a postnasal mirror will identify large adenoids. Investigations The only reliable means of assessing the size of the adenoid is examination under general anaesthetic. Besides snoring.ADENOIDS The adenoids are a mass of lymphoid tissue found at the junction of the roof and posterior wall of the nasopharynx. The size of the adenoids varies. but some preoperative investigations may suggest enlargement. and unfortunately the parents’ history is not always reliable.

• Persistence of symptoms. Sleep apnoea. • Cleft palate.8 OTOLARYNGOLOGY proportion in relation to the size of the airway. Otitis media with effusion (glue ear). Soft palate damage. an adenoidectomy is only indicated if troublesome symptoms can be attributed to abnormal adenoid hypertrophy. • Subluxation of the atlanto-occipital joint (secondary to infection). Recurrent acute otitis media. 2. • • • • Anaesthetic complications. Chronic rhinosinusitis. 3. Indications for adenoidectomy Generally speaking. Dislocation of the cervical spine. Immediate. If enlarged adenoids are present they can then be curetted. • Hypernasal speech (rhinolalia aperta). Reactionary haemorrhage. • Eustachian tube stenosis. All children who have a bifid uvula should have a submucous cleft excluded. Contraindications for adenoidectomy • Recent upper respiratory tract infection. This is not always accurate and some children will still need an examination of the postnasal space under general anaesthetic. . • An uncontrolled bleeding disorder. The indications for adenoidectomy are as follows: • • • • • Nasal obstruction. Late. Intermediate. Complications 1. They should never be removed in a child who has had a cleft palate repair or a congenitally short palate. • Secondary haemorrhage. The adenoids assist in closure of the nasopharynx from the oropharynx during speech and deglutition.

p. Follow-up and aftercare In view of the problems with accurate diagnosis and the potential long-term complications it is worthwhile reviewing adenoidectomy children in the outpatient clinic 6 months postoperatively. Related topics of interest Otitis media with effusion. . A postnasal pack should be inserted if necessary. Snoring and obstructive sleep apnoea. p. 1992. 333. 297. p. 213. Current Opinion in Otolaryngology and Head and Neck Surgery. Advances in adenotonsillar disease. Tonsillectomy. Silva AB. Some surgeons advocate removal of the upper part of the adenoid mass leaving a lower ridge of adenoid tissue against which the defective palate may continue to make contact. p. Tonsil diseases. 13:259–264. Assessment and treatment of adenotonsillar hypertrophy in children. This is treated in the same manner as posttonsillectomy haemorrhage. It often improves with time and speech therapy but may be sufficiently severe to require a pharyngoplasty to correct the problem. Hypernasal speech can be a troublesome complication in some children. Potsic WP. 1:177–184. Further reading Hotaling AJ. 330. The child should be returned to theatre and an attempt made to localize and diathermy the bleeding point. American Journal of Otolaryngology.ADENOIDS 9 The most serious complication is reactionary haemorrhage. 1993. It is less likely to occur if children with palatal abnormalities are excluded from operation.

Long-standing cases of perennial allergy may not display all these features. The IgE antibody is composed of an Fc and an Fab portion. so forming a cross-link composed of IgEallergen-IgE. but they often have nasal obstruction due to hypertrophy of the turbinates sometimes associated . Aetiology Allergy is a hypersensitivity reaction of tissues to certain substances called allergens. associated with itchy and watering eyes. Pathogenesis Immunoglobulin E is formed by plasma cells which are regulated by T-suppressor lymphocytes and Thelper cells. type 1 hypersensitivity reaction in the mucous membranes of the nasal airways. the ground substance viscosity is reduced by enzymes such as hyaluronidase. oedema. This produces the typical features of vascular congestion. The disease is very common.forinae) and animal epithelia. Typical allergens include pollens. The patient suffers from rhinorrhoea. This triggers a chain of events with the synthesis and release of arachidonic acid metabolites (prostaglandin D. house dust mite (Dermatophagoides pteronyssinus and D. proteases and more chemotactic factors). The commonest allergens are highly soluble proteins or glycoproteins with a molecular weight in the range of 10000–40000. It can be either seasonal (summer hayfever) or perennial (sometimes with seasonal exacerbations). leukotrienes and other chemotactic factors) and initiates disruption of the mast cell with degranulation of lysosomes (releasing histamine. moulds. Clinical features Seasonal rhinitis usually occurs any time from early summer to early autumn depending on the specific allergen. nasal irritation and sneezing. The allergen is thought to interact with two adjacent cellbound IgE antibody molecules. which have receptors for the immunoglobulin on their cell membrane. The effect is that capillaries become more permeable.ALLERGIC RHINITIS Allergic rhinitis is an IgE-mediated. The Fab portion of IgE is free to combine with an allergen. In allergic patients the IgE Thelper cells appear to promote overproduction at times of exposure to the allergen. In normal individuals this system maintains a constant function. affecting approximately 30% of the Western population. eosinophils infiltrate the tissues and oedema occurs. or suppressor T cells may not be functioning correctly. rhinorrhoea and irritation. Some individuals (described as atopic) will have a strong family history of allergy or a previous history of eczema or asthma. The Fc portion of IgE has an affinity for mast cells and basophils.

The epidermal prick test and the intradermal injection test use an allergen placed on the skin of the flexor aspect of the forearm. Total plasma IgE levels may be measured in the plasma radioimmunosorbent test (PRIST) and IgE to specific allergens in the radioallergosorbent test (RAST). Some patients still prefer the older antihistamines which may cause drowsiness (e. If an adverse reaction occurs. . However. the nasal mucosa classically appears moist. azelastine hydrochloride) have the advantage of minimal systemic absorption. a tourniquet should be placed proximally to contain it and the patient given intravenous hydrocortisone. etc. pale and swollen. Polyps may be present. Topical steroid sprays and drops are now considered to be the cornerstone in the treatment of rhinitis. mometasone. astemizole. loratidine). 2. as is the chance of promoting fungal infections. 4. but clinically the most useful are the skin tests and plasma IgE measurements. Sometimes the mucosa is red and the turbinates may have a blue hue. house dust mite.g. cetirizine. Examples include fluticasone. On examination. fexofenadine. animal epithelia.g. Specific substances can be used depending on the history. Crusting and bleeding are the main side-effects. and triamcinolone sprays. If the patient is highly sensitive a widespread or even an anaphylactic reaction may result.g. Systemic absorption is negligible. Nasal smears. 3. 1. Skin tests. An eosinophilia may occur in an acute allergic reaction but is unusual in allergic rhinitis.g. Oral antihistamines which selectively block histamine receptors. These tests are more convenient. Oral steroids are similarly indicated. Avoidance of the precipitating allergen is obviously helpful. Depot intramuscular injections of steroids (e. cause minimal or no drowsiness and can be given once daily are now available (e. but only in short courses. school examinations). A battery of common allergens (e.The effect can be measured objectively by rhinomanometry.). 2. triamcinolone acetonide) should be reserved for when symptoms interfere with special events (e. and the turbinates hypertrophied. A drop of the suspected allergen squeezed into the nose may cause symptoms (rhinorrhoea. Investigations There are many investigations available. 4. Provocation tests. chlorpheniramine (chlorphenamine) and adrenaline (epinephrine). etc. Resuscitation equipment must always be available although the epidermal prick test is safe if properly performed. sneezing. Intranasal antihistamine sprays (e. pollens. 3. Blood tests.) are compared with the controls by the wheal they produce.g. A negative control (carrier substance) and a histamine-containing solution (positive control) are used to ensure that the patient is not allergic to the carrier substance and does react in the normal fashion to histamine. They are safe and effective.ALLERGIC RHINITIS 11 with hyposmia. Patients with perennial rhinitis are almost invariably allergic to house-dust mite and typically have more than one allergy. they are more expensive and have no diagnostic superiority over skin tests. but not always possible. feathers. If the patient has an allergy to this then a wheal and flare will come up within 20 minutes.g. An increase in eosinophils in a nasal smear indicates an allergic rhinitis but is not diagnostic. chlorpheniramine and triprolidine) and they should be warned of this. moulds. do not expose the patient to the risks of the skin tests and do not rely on the use of a specific allergen. Management 1. but they are more often seen in intrinsic rhinitis.

It has few side-effects. Current Opinion in Otolaryngology and Head and Neck Surgery. but needs to be used five to six times per day for adequate prophylaxis. Developments in the drug treatment of allergic rhinitis. but may be effective in children and can be used for allergic conjunctivitis. ipratropium bromide) are useful in the treatment of patients in whom rhinorrhoea is the predominant symptom. 285.g. p.g. 1998. 1985. Journal of Allergy and Clinical Immunology. 6. deflected nasal septum or turbinate hypertrophy) or concomitant disease of the sinuses that complicate and exaggerate the symptoms of the rhinitis. Desensitization involves a series of injections of small amounts of the proven allergens in a purified form. When there are any nasal abnormalities (e. Leukotriene synthesis inhibitors and receptor antagonists are not marketed for the treatment of allergic rhinitis. The main complication of this treatment is anaphylaxis. Topical anticholinergic drugs (e. in particular pollen allergy. Sodium cromoglycate stabilizes mast-cell membranes and therefore prevents the release of the allergic response mediators. chlorpheniramine and adrenaline. Intrinsic rhinitis. 9. Baroody FM.12 OTOLARYNGOLOGY 5. in the hope that blocking IgG antibodies will be produced. 7. so compliance is poor. . p. they should be treated on their own merit. 8. Related topics of interest Sinusitis. If the offending allergen is identified by any of the tests then the patient should be given general advice on avoidance. Further reading Norman PS. especially turbinate surgery when there are symptoms of nasal obstruction. 6:6–17. Follow-up and aftercare Most cases of allergic rhinitis can be managed by the patient’s general practitioner. It is really only of use in patients who are sensitive to only one or two allergens. 131. Resuscitation equipment must always be available where this therapy is performed. Allergic rhinitis. and in case of anaphylaxis there must be a supply of intravenous hydrocortisone. Surgical treatment has a role to play other than in symptom control. and for this reason its use in the UK has been discouraged. but they show promise for the future treatment of the disease. It works in relatively few people. 75:531–545.

Routine haematological and biochemical investigations are generally limited to the following: . Obstructive sleep symptoms and a history of nocturnal apnoeas are easily overlooked on routine clerking. especially bronchodilators. • free from pain post-operatively. In these cases a thorough medical workup will assess risk and potential for improvement prior to surgery. Liaison between the surgeon and anaesthetist is mandatory to anticipate and minimize critical operative events. Airway assessment by clinical. blood or infected material). Cardiovascular workup may require referral for left ventricular function assessment by echocardiography and exercise tests in angina patients. there are also quite lengthy procedures performed on rather infirm elderly subjects. Safety during the procedure depends on the pre-morbid medical state of the patient. Pre-operative assessment Most ENT surgery can be regarded as relatively superficial procedures performed on fit young patients. At the other extreme. fibreoptic and radiological imaging should involve the anaesthetist in that the appropriate measures for operative management should be planned rather than haphazard as a result of insufficient information.g.Charters Principles In providing general anaesthesia for ENT surgery an anaesthetist will aim to render a patient: • unresponsive to the stress of the surgical stimulus. Nutritional correction by naso-gastric or parentral feeding may substantially improve pre-operative status of patients with swallowing difficulty. the anaesthetist must ensure continuous patency and adequate measures to deal with any contamination (e. It is important to determine pre-operatively which patients should be singled out for post-operative oximetry monitoring and the setting most appropriate for their nursing care. • amnesic for the event. effect of the anaesthetic agents used and the particular requirements of the surgery. Upper airway tumours are associated with longstanding cigarette consumption and patients who have already suffered for many years from chronic pulmonary and cardiovascular disease.ANAESTHESIA—GENERAL P. Optimization of pulmonary function may be helped with pre-operative physiotherapy and medications review. When surgery involves the airway itself.

Oral sedative agents are often used in children and local anaesthetic cream (e. Medical treatments should be optimised preoperatively. e.g. hypertension.14 OTOLARYNGOLOGY • FBC (females of menstrual age. patients over 60 years. Premedication Premedication may be used to reduce anxiety and decrease the incidence of nausea and vomiting. Anticholinergics may be given as an anti-sialogogue. These guidelines are modified for the less well patient. and thus diffuses into air-containing spaces such as the middle ear. renal or hepatic impairment. after significant blood loss). Nitrous oxide (N2O) This has been in use for 120 years as a general anaesthetic. although patients with a compromised airway should not be sedated and appropriate reassurance may be an alternative. Steroid cover is required when patients have received steroids in the past 12 months and antibiotic prophylaxis for patients with valvular heart disease. Urea and electrolytes are mandatory when deliberate hypotension is to be part of the anaesthetic technique. Anaesthetic agents and technique The usual intravenous agents to induce anaesthesia are thiopentone. • Chest radiography (patients with cardio-respiratory symptoms. A benzodiazepine with an anti-emetic is a suitable combination. prior to major operations. or on medications such as diuretics and anti-hypertensives). etomidate and propofol.5%) is applied to potential venepuncture sites under an occlusive dressing. This is maximal after 40 min of anaesthesia and is implicated in the adverse positioning of grafts.5% with prilocaine 2. • ECG (patients over 60 years. enflurane. Hospitals normally have prescribed protocols for peri-operative care of diabetic subjects. It is 35 times more soluble in blood than nitrogen. • U&E (patients over 60 years. They are not given if hypotension is required as the resulting tachycardia antagonizes this effect. Total intravenous anaesthesia’ refers to techniques where the use of inhalation agents are avoided and drugs combinations such as propofol and remifentanil (a very short acting opiate) are administered by infusion pump. Induction of anaesthesia by breathing volatile anaesthetic agents remains common in paediatric practice where halothane and sevoflurane are usually preferred. isoflurane or desflurane in a mixture of nitrous oxide in oxygen. . Use of muscle relaxants in patients with difficult airways can lead to disaster when patients are rendered apnoeic and assisted ventilation is not possible.g. patients with diabetes. a eutectic mixture of local anaesthetic: lignocaine 2. EMLA. leading to an increase in pressure. Patients at risk of aspiration or gastric contents on induction of anaesthesia usually have a rapid induction sequence with cricoid pressure applied. These drugs are all short-acting and it is usual to continue anaesthesia by a volatile anaesthetic agent. cancer screening especially in patients with upper airway tumours). glycopyrolate being the best as it causes less tachycardia and does not cross the blood-brain barrier thus avoiding confusion. cardiac symptoms including palpitations and fainting). Pharmacological muscle paralysis is not usually mandatory for ENT surgery but can be used to facilitate tracheal intubation and to lessen the requirement for ‘deep anaesthesia’ with volatile agents alone. prior to major operations.

Induced hypotension This can reduce blood loss during head and neck operations. if ever. the avoidance of hypertension during laryngoscopy and intubation. warranted in ENT surgery. Nitrous oxide may be excluded by substituting air or by total intravenous anaesthesia. . Specific drugs used to induce hypotension include: • sodium nitroprusside. ECG. It may result in cerebral or myocardial ischaemia and renal or hepatic hypoperfusion. anaemia. central venous cannulation and bladder catheterization. blocks ganglia and directly reduces peripheral vascular resistance. volatile agent-induced vasodilatation. which releases histamine. the use of head-up positioning to encourage venous drainage from the operative site.g. 8 mg per 100 ml) which favours blood flow through free flaps versus higher levels which may improve oxygen delivery. • labetolol. • soiling (by blood or infected material). This should also apply when hypotensive anaesthesia is planned. non-invasive BP and pulse oximetry). • glyceryl trinitrate. Per-operative monitoring Apart from recommended minimum standards (HR. Care of the airway The airway can be a particular problem in ENT operations and difficulties may be due to: • morphological derangement. ischaemic heart disease. Large-bore intravenous access (to allow fluid correction of precipitous fall in blood pressure) and an arterial cannula for direct blood pressure monitoring are required if profound hypotension is to be induced. hypovolaemia or impaired renal or hepatic function. Blood loss measurement peroperatively often simply involves weighing swabs and measurement of the suction container. useful in preventing the reflex tachycardia seen in response to hypotension). Ideal postoperative haemoglobin is a compromise between a low haemoglobin (e. Techniques of inducing hypotension include: • • • • the prevention of anxiety-related tachycardia by good premedication. It has been suggested that packing the middle ear during surgery reduces the clinical significance of nitrous oxide-induced pressure changes.ANAESTHESIA—GENERAL 15 altered appearance of the tympanic membrane and postoperative nausea and vomiting. It is contraindicated in patients with coexisting hypertension. rarely. • trimetaphan. which dilates capacitance vessels. which directly dilates arterioles and venules. This is however. pregnancy. major operations will usually require invasive blood pressure monitoring. which reduces arteriolar tone (by its alpha-blocking effect) and heart rate (by its beta-blocker effect. previous cerebrovascular accident.

By comparison.g. Surgical debulking may be augmented by intravenous steroids and antibiotics. infection or haemorrhage into normal or abnormal tissue. laryngeal laser surgery and tumour debulking). This usually proceeds shortly after the histology becomes available. i. i. Management of these cases does depend on the experience of the doctors concerned. the use of airway devices such as the laryngeal mask airway (LMA) and cuffed oro-pharyngeal airway (COPA) may help to control the immediate airway difficulty. In all these situations the most important aspect is that the anaesthetist be as fully informed of the situation as possible pre-operatively. when the airway will be adequate in the post-operative period. This is used in patients presenting with acute airway obstruction where the immediate surgical aim is to improve the airway and acquire histology before considering formal treatment. When general anaesthesia is considered necessary the anaesthetist will usually consider techniques which allow sedation to be gradually increased. Post-operative care needs to be in an environment where the nursing and medical staff are aware of the risk of post-operative problems and their management.e. Because the view with a fibreoptic laryngoscope can be quite restricted. It should also be remembered that there is no guarantee that the trachea and in particular the subglottis will be free of pathology when there has been little time for formal investigations. Where airway instrumentation does need to be considered. Surgery for abscesses involving part of the upper airway must always be seen in context. pinhole glottis narrowing is not infrequently encountered. oedema. Tumours that are papilliferous are easier to debulk than sessile ulcers. acute obstruction is usually associated with a more ‘fluidic’ processes such as friable or cystic tumours. sessile ulcerative tumour and granulation/deposition diseases). the Aintree intubation catheter) over a fibreoptic laryngoscope. In the case of the airway worsening. relief of symptoms should be considered while determining what investigations are feasible. Acute airway obstruction usually means that the patient presents with an airway that is not severely narrowed. when airway obstruction has been longstanding (weeks or months). the sedation can then be lightened and if necessary the patient is woken up. . fibrosis following radiation treatment. Helium and oxygen mixtures may relieve symptoms as may bronchodilators and nebulised adrenalin. Anxiety can potentiate as well as result from respiratory difficulty and reassurance may help but even small dose of anxiolytic can induce respiratory arrest. Then either can be used as a means to tracheal intubation using an exchange catheter (e. Experience will guide in the choice as to whether or not awake fibreoptic laryngoscopy should be considered. the endoscopist needs to have a good general idea as to where to expect to find the relevant anatomical landmarks. Where a patient presents acutely in a state of distress. However. Airway debulking is a particular problem for the anaesthetist.g. adaptation over time may mean that very small airways are encountered.16 OTOLARYNGOLOGY • surgery to alter the airway itself (e. Patient co-operation is important when sedation is inadvisable. The surgeon and anaesthetist need to agree on a suitable end point for this surgery. In young children and adults less than 30 years of age. Tracheotomy under local anaesthesia is commonly regarded as a final fallback position but success may be difficult in an extremely restless patient who is fighting for breath. If the airway pathology is not a relative contraindication. The nature of the relevant pathology is important because chronic obstruction tends to be a relatively ‘solid’ processes (e.e. good radiological imaging may delineate precise morphological changes and also indicate where the abscess wall is thinnest and in danger of disruption. Bleeding after surgery is possible as is the risk of laryngeal oedema. External drainage under local anaesthesia may be appropriate and normally negates the risk of airway contamination. Antibiotics alone may resolve some situations and good drainage will usually only be effective in well organised abscess cavities. even with mild stridor a 4-mm microlaryngoscopy tube can usually be advanced into the trachea.g.

p. Paediatric airway problems. wrapped in aluminium foil or laser-proof. p. The tracheal tube cuff is filled with saline or preformed with foam. Related topics of interest Anaesthesia—local. Tracheostomy. the surgery must be discontinued and ventilation stopped until the fire is extinguished with a pre-filled syringe of saline. 19. 138. If airway fire occurs. the patient ventilated with 100% oxygen. . 124. The tracheal tube should be flexo-metallic. a bronchoscopy performed. Hypopharyngeal carcinoma. steroids commenced and antibiotics and prolonged ventilatory support provided as necessary. Stridor and stertor. p. p. 311. Laryngeal carcinoma p. p.ANAESTHESIA—GENERAL 17 Laser surgery carries a risk of an airway fire after ignition of the tracheal tube or the fresh gas mixture. 336. The tracheal tube should then be replaced. 232.

more of the drug remains in the ionized form. Classification There are two broad classes of LA: • esters (e. At a low pH. Where the circulation is poor or when vasoconstrictors (e. ropivacaine and levobupivacaine). . cocaine and procaine). lignocaine. ability to penetrate mucous membranes and duration of action. Manifestations of toxicity usually start during drug administration or very shortly afterwards. water solubility. perioral paraesthesia. slurred speech. tinnitus. Toxicity. Complications Complications associated with the use of local anaesthesia may not be common but can be life threatening and for this reason their use should be restricted to areas where resuscitation facilities are to hand.g. larger doses can be tolerated. • amides (e. toxicity most commonly results from inadvertent direct intravascular injection or rapid absorption via mucous membranes and toxicity from any concomitant vasoconstrictor is likely.ANAESTHESIA—LOCAL P. convulsions and coma. facial twitching. preventing it from diffusing across the axonal membrane and therefore reducing efficacy. adrenaline) are administered with the LA. benzocaine. metabolism or dilution which reduce local tissue concentration of the LA to restore nerve function. For ENT surgery. 1.Charters Mode of Action Local anaesthetic (LA) agents produce a reversible block in the transmission of impulses along nerve fibres. They vary in terms of potency. diffusion.g. toxicity. bupivacaine. The blood supply may be increased in infected tissue where the choice of local anaesthesia must be questioned. When applied to different sites their efficacy is influenced by these properties and the local blood supply can have implications for both duration of action and liability to toxic effects.g. They include: • CNS: lightheadedness. This depends on the dose of the agent and speed of uptake into the circulation. Local anaesthetics are weak bases and the degree of ionization depends on the individual drug’s pKa and the surrounding pH. prilocaine. Removal from the site of action tends to be by the circulation.

Toxic effects are usually self-limiting but fitting and cardiovascular collapse should be treated with oxygen administration. Lignocaine. Duration of action (when infiltrated): 90 min without adrenaline. Duration of action: 30–60 min. Cardiopulmonary collapse requires ventilation with 100% oxygen. Levo isomers of amide local anaesthetics in general tend to have lower potential for systemic toxicity than the dextro forms. Reactions are more common with esters than amides. drug administration should be stopped immediately and the situation assessed. Maximum dose: 5 mg/kg or 7 mg/kg with adrenaline. Clinical manifestations include cardiovascular collapse. sprays as 4% or 10% and ointments of 2–5%. It has vasoconstrictive properties and is rapidly effective on mucous membranes. It potentiates catecholamine activity and sensitizes the myocardium to adrenaline. Anyone who has had a severe reaction should be observed on a High Dependency or Intensive Care Unit to monitor cardiovascular and renal function even when immediate recovery appears complete. necessitating prolonged cardiac massage. hypoxia and respiratory arrest.ANAESTHESIA—LOCAL 19 • CVS: bradycardia. Continuing care (or observation and monitoring in the case of apparent recovery) in ICU or HDU is mandatory. useful for postoperative analgesia. At toxic levels cardiac events. CPR may be required. hypotension and cardiac arrest. Ropivacaine is said to produce less motor block for the equivalent sensory block to bupivacaine. 3. Max dose: 2 mg/ kg or 3 mg/kg with adrenaline. 5. • RS: an initial increase in respiratory rate followed by respiratory depression. bronchospasm. Levobupivacaine. may precede neurological events. A vasodilating amide with a long duration. It is available in injectable form as 0.5–2%. IV fluids and adrenaline 1:10000 in 1 ml aliquots. Maximum dose: 3 mg/kg or 7 mg/kg with adrenaline. generalized (and laryngeal) oedema and there may be an urticarial rash. A single isomer and propyl homologue of bipivacaine (itself a racemic mixture). Duration of action: 240 min without adrenaline. . An ester hydrolysed by plasma cholinesterases. The airway should be secured and the subject positioned horizontally. An amide with no vasodilating effect and lower systemic toxicity. Bronchodilators may be required. Cocaine. The single levo isomer of bupivacaine which has been shown to have less systemic toxic effects. bupivacaine) can have a prolonged effect on the heart. Longer acting drugs (e. Specific LA agents 1. 2.g.g. If any of these symptoms occur during the injection. e. Maximum dose 1. Prilocaine. Allergic reactions. The dosages are similar. Bupivacaine. especially ventricular fibrillation. Ropivacaine. adrenaline 1:200000. The onset of a reaction is more immediate and more severe with inadvertent intravenous administration. Metabolism to otoluidine may cause methaemoglobinaemia.5 mg/kg or total 100 mg in a fit adult. 2. The sensory block lasts longer than that with bupivacaine used in similar dosages. Antihistamines should be considered and if hypotension and bronchospasm persist steroids should also be considered. An amide metabolized in the liver. Concern about toxicity has recently restricted its availability to a 10% spray used topically to facilitate nasal surgery. Duration of action: 140 min. It is a mild vasodilator and is often given with a vasopressor. 6. 4.

Vasopressors are contraindicated in sites supplied by end arteries. LA used on its own or combined with general anaesthesia. Nose. Alternatively. LA is used for direct laryngoscopy or awake intubation. ribbon gauze soaked in LA is packed into the nose and left for 10 min. Additional anaesthesia may be supplied by anterior ethmoidal or maxillary nerve blocks or by infiltration of the columella. Anaesthesia for tracheostomy is by field infiltration with progressive supplementation. (b) Cricothyroid injection. An initial cricothyroid injection can reduce coughing when the trachea is incised. A 2-ml volume of 4% lignocaine is injected via the cricothyroid ligament after aspiration of air to confirm needle placement. two wool applicators soaked in LA are applied. A small intravenous cannula with the needle removed avoids needle stick injury to the posterior tracheal wall during the coughing on injection. (a) Modified Moffet’s technique. • Percutaneous—2 ml of LA is injected where the nerve divides at the greater cornu of the hyoid. hypertension or thyrotoxicosis and in those on monoamine oxidase inhibitors. 2. • Krause’s method—a swab soaked in 4% lignocaine is held. larynx and trachea. The nasal cavities are sprayed with LA and the patient placed supine with the head extended over the end of the trolley.20 OTOLARYNGOLOGY Vasoconstrictors Combined with a LA agent these reduce the risk of systemic toxicity and intraoperative bleeding and prolong the duration of action. A 2-ml volume of 5% cocaine is applied to each nasal cavity using a specially angulated cannula. After applying LA to the nasal cavity.5%) is a used topically in the nose and is also available combined with lignocaine. sensitises the myocardium to adrenaline and concomitant use is better avoided. Pharynx. Phenylephrine (0. Vasopressors are contraindicated in patients with ischaemic heart disease. a volatile anaesthetic agent. Ear. one to the region of the sphenopalatine foramen and the other to the anterior end of the cribriform plate. Local anaesthetic uses in ENT surgery 1. (b) Nasal pack. . 3. Infiltration may be supplemented by: (a) Auriculotemporal nerve block—2 ml of lignocaine is injected anterior to the meatus. When using a fibreoptic bronchoscope LA is sprayed as the scope is advanced. After removal of the pack. Halothane. After 10 min the nose is pinched and any remaining solution removed. by Krause’s forceps. the following blocks may be used: (a) Superior laryngeal nerve. The oropharynx is anaesthetized by spraying or nebulizing 4% lignocaine. in each piriform fossa for 1 min. or using a benzocaine lozenge.

ANAESTHESIA—LOCAL 21 (b) Greater auricular nerve block—2 ml of lignocaine is injected 2 cm both anterior and posterior to the tip of the mastoid. p. 14. Related topic of interest Anaesthesia—general. .

for example teeth. lined only with squamous epithelium. (f) Reactive neck lymphadenopathy. (e) Salivary gland tumours. Epidermoid cysts. Cystic hygromas usually arise in the lower neck. There are three types: 1. (g) Neck space infection. and cystic hygroma (cysts of varying sizes). (b) Developmental: branchial cysts. . 3. Simple and cavernous lesions arise principally in the lips. endodermal and mesodermal elements. cheek and floor of the mouth. Teratoid cysts are lined by respiratory or squamous epithelium and contain ectodermal. This chapter describes congenital. Dermoid cysts These are midline swellings that do not move with swallowing or tongue protrusion. Congenital Lymphangiomas There are three types of lymphangioma: simple (thin walled channels). nails or thyroid tissue. (c) Tumours of the parapharyngeal space. Injection of sclerosants and radiotherapy have been suggested but are not recommended. 2. cavernous (dilated lymphatic spaces). developmental and parapharyngeal-space lumps. Treatment is by surgical excision. thyroglossal cysts.BENIGN NECK LUMPS Classification (a) Congenital (defined as present at birth): lymphangiomas. laryngoceles. True dermoids lined with squamous epithelium and all other normal skin appendages. dermoids. (d) Thyroid swellings. The last four groups above are discussed as separate topics elsewhere in the book. pharyngeal pouches.

They arise from elements of squamous epithelium within a lymph node. Many experts therefore recommend a 99mTc or radio iodine (131I) uptake scan prior to excision. sneezing or . They usually present in young adults. expanding internally to present in the vallecula or externally through the thyrohyoid membrane. are recommended. A long course of antibiotics and repeat aspiration of the cyst. They are remnants of the cervical sinus. Following this procedure the recurrence rate varies from 2% to 8%. Excision should only be attempted when all inflammation has settled to minimize the risk of rupturing the cyst wall. Ninety per cent of thryoglossal cysts are midline and 9% left-sided. If the hyoid body is not removed the recurrence rate rises to 85%. which may lead to a recurrence or. Most occur in childhood (mean age 4 years). The body of the hyoid and preferably a wedge of tongue base should therefore be included in the excision of the cyst (Sistrunk’s Procedure). Thyroglossal cysts should not be incised and drained as this may cause an ugly sinus which is difficult to excise in toto and in continuity with the deflated cyst. if the child allows. 2. a fistula. The tract may climb anterior or posterior to the body of the hyoid to the tongue base. They arise from the laryngeal saccule. occurring between the body of the hyoid bone and the cricoid cartilage. pain and tenderness. Branchial cysts are lined by stratified squamous epithelium and contain lymphoid tissue in their wall. 80% in men with a mean age of 55. They are remnants of the duct connecting the thymus to the third pharyngeal pouch. Most arise along the line of the deep cervical lymph nodes deep to the anterior border of sternomastoid at the junction of its upper third and lower two thirds. coughing. Developmental Branchial cysts Four theories regarding aetiology have been proposed: 1. In a patient over the age of 40 years a metastatic node must be excluded. if wall remnants are left. In most subjects raising the intralaryngeal pressure causes no expansion of the saccule. 3. perhaps because of a wider than usual true cord to false cord distance (wide neck) or because the false cord is compressed against the saccule to create a one-way valve. 60% on the left and 60% in males. They move with swallowing and tongue protrusion as they are ultimately attached on their deep aspect to the larynx. Infection causes the rapid onset of diffuse swelling. In those in whom the saccule expands. 4. They arise from remnants of the first pharyngeal pouch. Diagnosis is by clinical examination and from fine needle aspiration biopsy. This is the current consensus view. They may contain elements of thyroid tissue and may even be the sole source of functioning thyroid tissue. Laryngocele Only about 30 occur each year in the UK. A quarter of branchial cysts become infected and should be managed similarly to an infected thyroglossal cyst. although an ultrasound scan is less invasive and will allow confirmation of whether there is a normal gland present.BENIGN NECK LUMPS 23 Thyroglossal cysts These are cysts along the tract of the obliterated thyroglossal duct.

if it involves the ganglion nodosum just below the jugular foramen. vagal. Neurogenous tumours. occurs in chemodectomas of these three sites. syncope. or laterally to present in the upper deep cervical region. Carotid aneurysm. Parotid deep lobe tumours. the glomus vagale tumour. but paralysis is unusual. Parotid tumours are the commonest and are discussed elsewhere (see Related topics). and glossopharyngeal. . (b) Schwannomas are benign tumours of the neurolemma or sheath of Schwann and so tend to be encapsulated. In the parapharyngeal space a painless neck mass is usually the only sign. which. Their expansion may compress the involved nerve. They are occasionally associated with a ventricular carcinoma. although with the vagal nerve paragangliomas pulsating. giving rise to reduced function. accessory and hypoglossal nerve palsies may arise if the tumour expands at the skull base. Malignant change rarely. Parapharyngeal tumours expand either medially. Patients present with a slow-growing painless lump in the neck or a mass pushing the tonsil medially.24 OTOLARYNGOLOGY trumpet playing may fully develop the laryngocele. Plain anteroposterior and lateral neck radiographs may show an air-filled sac. tinnitus. Vagal paragangliomas arise from paraganglionic tissue within the perineurium of the vagus. the common tumours are: • • • • Lipomas. Neurogenous tumours develop from neural crest cells which have differentiated into Schwann cells or sympathicoblasts. sometimes causing weakness or paralysis of the involved nerve. Indirect laryngoscopy may reveal fullness of the ipsilateral false cord. which includes the upper half of thyroid cartilage on the side of the laryngocele so that its neck can be ligated. An intermittent neck swelling is the usual presentation. Laryngoceles may obstruct the larynx. (c) Chemodectomas arise from paraganglionic tissue at three common sites in the neck. Chemodectomas may occur rarely at other sites. However. these carotid body tumours are rare except in high-altitude population centres such as Mexico City. The cells are not functionally active. Schwann cells give rise to neurofibromas and schwannomas. glomus vagale and glomus jugulare tumours). when the tonsil will be displaced towards the midline. Tumours of the parapharyngeal space This space is described in Neck space infection (p. Carotid body tumours may be pulsatile with an audible bruit. perhaps with hoarseness. 188). is referred to as a glomus jugulare. On the medial side of the carotid bulb are found highly vascular tumours arising from the carotid body cells. (a) Neurofibromas arise from endoneural fibrous connective tissue and are composed of a mass of spindle cells which can entwine nerve fibres. particularly the larynx. It is usually impalpable but may become both visible and palpable on performing the Valsalva manoeuvre. the sympathicoblasts to ganglioneuromas and chemodectomas (carotid body tumours. It is therefore important to exclude a metastatic node as a cause of the swelling. cough or pain. Occasional reports of metastases in the literature may be confusing a chemodectoma with a large-cell neuroendocrine carcinoma. if ever. so the safest treatment is excision.

Glasscock ME et al Diagnosis and management of paragangliomas of the skull base. Follow-up and aftercare Review of all parapharyngeal mass patients postoperatively for 5 years. A tissue diagnosis may not be possible. American Journal of Surgery. Head and Neck Surgery. 159:389–393. if necessary under CT guidance.BENIGN NECK LUMPS 25 A carotid aneurysm may be caused by atheroma. 354. all of which must be known prior to surgery. A significant proportion of young patients will refuse surgery if presented with all the facts. trauma or infection. There is also a small. . but definite. The vagus and the hypoglossal nerves are at risk of injury. may allow a definite diagnosis to be made. 7:32–43. Under no circumstance should either a Tru-cut biopsy or a biopsy from within the mouth be attempted because the vascularity of a carotid body tumour may cause a rapidly expanding parapharyngeal haematoma which might occlude the oropharyngeal airway. Salivary gland diseases. For these reasons. is indicated. Treatment The mass will as a rule continue to expand so that symptoms may progress. Jackson CG. p. 1984. surgery is the treatment of choice for parapharyngeal tumours. p. Head and Neck Surgeons. risk of stroke from surgery. A fine-needle aspiration biopsy. transparotid or transmandibular route. If a carotid body tumour is suspected a digital subtraction angiogram will allow precise definition of the tumour circulation. British Association of Otolaryngologists. Harris PF. Pesavento G. 274. If expanding or causing transient ischaemic attacks. except those who had a lipoma. although symptoms gradually settle. Second Consensus. Investigations An MRI scan will delineate the position and assess the size and vascularity of the mass. especially if an experienced speech therapist is involved in rehabilitation. Vocal cord palsy. The parapharyngeal space can be approached by either a transcervical. Effective Head and Neck Cancer Management. Assessment and treatment of neurogenic and non-neurogenic tumours of the parapharyngeal space. 1990. 188. Further reading Ferlito A. it can be resected and replaced with a reversed saphenous vein graft. its principal feeding vessels and the presence of a cross-circulation. p. Recher G et al. p. Related topics of interest Neck space infection. Glossopharyngeal and vagal nerve injury may give rise to aspiration and a hoarse voice. 2000. A vocal cord palsy is treated as discussed elsewhere (see Related topics of interest). Wilson J (ed). Recent publications have suggested that carotid body tumours may be radiosensitive and radiotherapy may be indicated either as adjuvant treatment or in those unfit or unwilling to have surgery. 271. Salivary gland neoplasms.

via a siphon tube and 14G cannula. Positional alterations and the presence of a caloric response in microgravity have led to suggestions that a direct thermal effect on the sensory organs may account for as much as one-third of the response. The inertia of the endolymphatic fluid means that there is a relative difference in the velocity of the canal and the fluid with head movements. A stopwatch is used to time the period from the . complex three-dimensional information is provided. the whole membranous canal is filled with endolymph. kept at these temperatures in two heated tanks about 1 metre above the test couch. although this in no way reduces the value of the test. It has become apparent in recent years that thermal convection currents are not the only component in the caloric response. The two labyrinths work in conjunction so that an increase in neural signals from one canal will be associated with a decreased discharge rate from the corresponding canal on the opposite side. Procedure The classic bithermal calorics utilize water at 30 and 44°C. After checking that the external canals are clear of wax and debris and that the tympanic membranes are intact. Background The caloric response can be used to test the integrity of this system and was first described by Robert Barany in 1906 and for which he was awarded a Nobel prize in 1914. The patient reclines on the couch at 30° above the horizontal so as to bring the lateral semicircular canal into the vertical position. As the three canals are mutually at right angles. This fluid movement leads to stimulation of the stereocilia and consequent nystagmus and vertigo. He postulated that altering the temperature of the endolymph sets up thermally induced convection currents. Each canal possesses a dilation at one end called the ampulla. for 40 seconds. Caloric testing was further refined in 1942 by Fitzgerald and Hallpike when they described a standardized bithermal caloric test which remains an essential vestibular investigation to this day. This results in fluid being forced through the gap between crista and cupula and a deflection of the stereocilia which causes either an increase or decrease in the resting tonic discharge depending on the direction of deflection. cold water (30°C) is run into the left ear. Within the ampulla exists a saddle-shaped crista upon which sits a gelatinous cupula.CALORIC TESTS Physiology The semicircular canals are paired sensory structures responsible for the detection of angular acceleration.

to predict the degree of vestibular activity. p. Cold tap water can be used as a very basic single temperature screening test. . This finding invariably implies a lesion of the peripheral vestibular system (e. Vestibular function tests. 1. This is easily remembered by the mnemonic COWS (cold-opposite. By the nature of the test a canal paresis or directional preponderance must be greater than 20–25% to be significant. • Unilateral canal paresis denotes that the response of one side to hot and cold stimuli is reduced or absent compared with the opposite side. as the tumour usually arises from the superior vestibular nerve and leads to an ipsilateral canal paresis. Exceptions to this include patients with lesions at the vestibular nerve-root entry-zone of the brainstem (e.g. Cold stimulation leads to nystagmus with the fast phase to the opposite side. British Journal of Audiology. 1995. Interpretation By definition. 350. Clinical indications Caloric testing forms the cornerstone of investigation for any vestibular pathology and is therefore useful in all patients with vertigo. 346. Further refinements can be added by the use of Frenzel’s glasses to remove optic fixation or measuring the nystagmus electrically (electronystagmography).g. the direction of the nystagmus is described by its fast phase. p. multiple sclerosis or lateral brainstem infarction). p. Although MRI scans are now the investigation of choice for an acoustic neuroma. caloric tests may still be of some value. Vertigo. 134. Further reading Luxon LM. based on the recorded times for each part of the standard caloric test. Labrynthitis. It suggests pathology. warm-same). Acta Otolaryngologica. Various formulae exist. Stahle J. horizontal canal or vestibular nerve on that side). The most common abnormalities found are canal paresis or directional preponderance (or a combination of the two). 109:162–167. p. Comparison of caloric nystagmus by observation of duration and by electronystagmographic measurement of slow-phase velocity. This procedure is repeated for the right ear and then for both ears with the warm water (44°C). Controversies on the caloric response. • A directional preponderance denotes a non-specific enhancement of nystagmus in one particular direction. 29:107–116. but is usually non-localizing (may arise from any part of the peripheral or central vestibular system). in which there is central pathology and also a canal paresis. A number of variations on this basic theme exist. 1990. when directional preponderance is usually directed away from the diseased ear. while warm stimulation leads to nystagmus with the fast phase to the same side.CALORIC TESTS 27 start of this manoeuvre to the point at which the nystagmus stops with the patient fixating on a point on the ceiling. It may be localizing with some peripheral lesions. Related topics of interest Acoustic neuroma. and in patients with perforated eardrums air may be used to supply the thermal stimulus.

infectious mononucleosis. • Level I. Inflammatory (sarcoidosis). Infectious (tonsillitis. The scans can also reveal the integrity or involvement of the vasculature by a metastatic lymph node. as well as pulmonary tuberculosis or mediastinal gland enlargement Anatomy The following definitions are recommended for the boundaries of cervical lymph node groups. false-positive results can occur with FNA. Neoplastic (primary arising from neck structures. Congenital or developmental (thyroglossal.CERVICAL LYMPHADENOPATHY Cervical lymphadenopathy implies disease involving the cervical lymph nodes. Cervical node status is one of the most important prognostic factors in the head and neck cancer patient. In a patient with positive nodal disease. Falsenegative and. examination including endoscopy. control of regional metastatic disease constitutes a significant part of the management of head and neck cancer. radiology and laboratory tests. An ultra-sound scan (with USS guided FNA) or MRI scan may delineate impalpable nodes. branchial and dermoid cysts). actinomycosis. A primary carcinoma arising in the upper aerodigestive tract may metastasize to the lymph nodes of the neck. 23). but specific details are found elsewhere (see Benign neck lumps. p. tuberculosis. the hyoid bone. Consists of the submental and submandibular lymph nodes within the triangle bounded by the anterior belly of the digastric. Fine-needle aspiration (FNA) cytology is probably the single most useful diagnostic procedure if a neoplastic lymph node is suspected. Therefore. the posterior belly of digastric and the body of the mandible. The specific investigations will be dictated by the differential diagnosis. The diagnosis is from the history. HIV). A chest radiograph may show a primary carcinoma or evidence of secondary spread. very rarely. the usual expected survival rate for any specific primary tumour is reduced by one half. In this topic a simple differential of these diseases is presented. metastatic secondaries. . 3. so the information must always be used in conjunction with the clinical findings. haematogenous). The remainder of the chapter is confined to the problem of neck node metastases. 4. Differential diagnosis Most cervical masses fall into one of four broad groups: 1. 2.

• Level IV (lower deep cervical). (a) Single ipsilateral node (3–6 cm in diameter). Postoperative irradiation to the neck following neck dissection is mandatory in the presence of ECS. • Level VI. Consists of the posterior triangle nodes which are located between the posterior border of the sternomastoid muscle and the anterior border of trapezius. Staging The staging system in most common use in the UK is that proposed by the International Union against Cancer (UICC). This information is only available after pathological staging (pTNM). the lymph node level and the presence of extra-capsular spread (ECS) are the most important prognostic parameters in metastatic disease of the neck. N0. The supraclavicular nodes are also included in this group. it has several inherent problems: clinicians will fail to agree on the presence of a palpable lymph node in as many as 30% of cases. Movable homolateral or bilateral nodes. 1. Fifty per cent of nodes with a diameter greater than 3 cm exhibit this. • Level V. Regional lymph nodes not palpable. it is generally acknowledged that the number of lymph nodes involved. Consists of lymph nodes around the middle third of the internal jugular vein extending from the carotid bifurcation superiorly to the cricothyroid notch inferiorly. Broadly speaking. Treatment The treatment of malignant neck nodes is by either some form of neck dissection or radiotherapy. The rupture of the lymph node capsule by tumour (ECS) is a bad prognostic sign. which is based on data developed by the American Joint Committee (AJC) for Cancer Staging. The performance of a neck dissection without palpable lymph nodes (prophylactic or elective neck dissection) is considered by some to be of doubtful value. The argument supporting dissection is that some lymph nodes may be invaded by tumour (occult nodes) and still be impalpable.CERVICAL LYMPHADENOPATHY 29 • Level II (upper deep cervical). Anterior compartment. Consists of lymph nodes located around the upper third of the internal jugular vein and adjacent spinal accessory nerve extending from the level of the carotid bifurcation to the skull base. Consists of lymph nodes located around the lower third of the internal jugular vein extending from the cricothyroid notch to the clavicle inferiorly. (b) Multiple ipsilateral nodes (up to 6 cm). Nodes > 6 cm in diameter. In addition. N3 Although this system is useful. (c) Bilateral or contralateral nodes (up to 6 cm). • Level III (mid deep cervical). lymph nodes of less than 2 cm diameter can be treated by radical radiotherapy and those greater than this size will be treated by a neck dissection with or without postoperative radiotherapy. NX N0 N1 N2 Regional lymph nodes cannot be assessed. Risk factors for occult nodes . Movable single homolateral node < 3 cm in diameter.

Supraclavicular nodes have the worse prognosis. It must be confirmed that the node is metastatic as a high proportion of nodes in this category do not contain tumour and. The incidence of further neck recurrence is probably reduced by postoperative radiotherapy. 4. if possible. physical examination. N3. The modality chosen is usually the same as that used for the primary tumour. Although recurrence after a course of radiotherapy can be treated by neck dissection. There is support for elective treatment of the neck or at least the first echelon nodes in tumours of these primary sites. or rarely. Larger nodes (N2a) and multiple ipsilateral nodes (N2b) are best treated by a modified or radical neck dissection because of the high incidence of ECR of the tumour and difficulty in sterilizing even small multiple nodes. Therefore a modified radical neck dissection is preferred by some surgeons for these patients. lung or stomach). extranodal spread is uncommon. base of tongue and pyriform fossa). This has the advantage of avoiding surgery and its morbidity. the size and histological grade of the primary tumour. 3. The use of radiotherapy also means that valuable prognostic information (pTNM) is not made available. Primary of unknown origin This term is applied to patients with a metastatic carcinoma in cervical lymph nodes with an ‘occult primary’. a modified radical neck dissection on the least invaded side. A careful search will usually reveal the primary tumour in the skin or mucosal surfaces of the head and neck. N1. The prognosis varies from a 30–70% five year survival. even if they do. ipsilateral tonsil excision. The prognosis depends on N Stage and position of the node. the survival after such salvage surgery is poor. 2. or the brachial plexus. N2. It is important to search thoroughly for the primary tumour by all available diagnostic methods including history. These nodes used to be referred to as ‘fixed’. Most surgeons advocate either staged bilateral radical neck dissection or. Prophylactic neck dissection has a place in the patient who has a primary tumour with a high incidence of occult nodes (nasopharynx. For other sites it is argued that no survival benefit is conferred and the morbidity/mortality of the operation outweigh the potential benefit. or the base of skull in the region of the mastoid process. in an area below the clavicles. Postoperative radio-therapy is indicated if there is ECR or positive margins in the resection specimen. If the tumour invades the internal jugular vein. The treatment can be by selective neck dissection or by irradiation. and little chance of cure. base of tongue. Many surgeons therefore adopt a wait and watch policy. but size is now the criterion for staging. Patients with a supraglottic carcinoma and bilateral nodes do better than those with cancer of other primary sites at high risk of bilateral neck metastases (base of tongue and hypopharynx). imaging. It is generally accepted that lymph nodes of less than 2 cm diameter can be sterilized by radiotherapy. panendoscopy and selective biopsies from high risk sites (nasopharynx. probably because many of these represent distant metastases from non-head and neck sites (e. although overall survival is not affected. The decision to treat should be taken very carefully as there is a considerable morbidity from a bilateral neck dissection which can be a simultaneous or a staged procedure. supraglottic larynx or oral cavity). Invasion of the carotid artery can be treated with a bypass procedure performed with the resection. tonsil. radiotherapy has its own morbidity and can only be used once.g.30 OTOLARYNGOLOGY are the site. it is almost certainly incurable. such as the lungs. but there is a high operative mortality. Fixation to the skin can be treated by resection of the tumour with involved skin which is replaced with the use of flaps such as a pectoralis major myocutaneous flap. In approximately 3–11% of cases the primary tumour remains elusive and it is for these that the term ‘primary of unknown origin’ should be reserved. pyriform fossa. Patients who have neck dissection and radiation therapy to both sides of the neck and the mucosal surfaces have better neck and local control than . However.

Squamous carcinoma presenting as an enlarged cervical lymph node. 185. Death by carotid artery rupture will usually ensue. Jones AS. Field JK. Annyas AA. p. Van Slooten EA et al. . Cancer. 19:63–69. These will help prevent colonization by anaerobes and alleviate the odour from tissue necrosis. 1993. p. Prognostic factors of neck node metastasis. Palliative therapy Patients with inoperable neck nodes that have fungated through the skin can be treated with local dressings of kaltocarb and topical metronidazole. Roland NJ. 7:185–192. The patient should always be treated with appropriate doses of opiate analgesia and antiemetics. Further reading Jones AS. Chemotherapy may have a place in improving this situation. 1994. The level of cervical node metastases: their prognostic relevance and relationship with head and neck squamous carcinoma primary sites. Clinical Otolaryngology. Phillips D. this does not seem to translate into prolonged survival. Neck dissection. 72:1756–1761. Clinical Otolaryngology. Snow GB. However.CERVICAL LYMPHADENOPATHY 31 those who do not have such extensive treatment. It is imperative that there is adequate social support and that the patient’s family doctor is aware of the situation if the patient is to be cared for in the community. Related topics of interest Benign neck lumps. Phillips DE. Roland NJ. Cook JA. 23. 1982.

half exhibit facial nerve palsies and one third of cases have laryngotracheal anomalies. Each nasal cavity is closed posteriorly by the thinned out posterior wall of the nasal sac. H. including the CHARGE association. The nose begins as two epithelial thickenings known as the nasal placodes. In addition. This refers to a problem of multiple congenital anomalies: C. which appear above the stomatodeum about the fourth week in utero. The diagnosis should be suspected immediately and an oral airway inserted to assist respiration. The condition may be unilateral (most commonly) or bilateral. . and there is a family tendency. and no airway can be demonstrated by holding a cold plated spatula below the nares—only the clear side steaming the surface (mirror test). The alae nasi dilate and the accessory muscles of respiration are used to no avail. obstructing the posterior nares. There is pallor and cyanosis until the mouth is opened and after a few quick breaths are taken the infant cries. ear abnormalities and deafness. This sequence of events continues. or both. R. A. This usually breaks down around the sixth week in utero. palate. called the bucconasal membrane. Clinical features A unilateral obstruction may be asymptomatic at birth but will later cause unilateral nasal discharge and obstruction. Examination of the nose will show a thick gelatinous secretion on the affected side. This is compressed to form the nasal septum as the lateral nasal processes approach each other. atresia choanae. The medial processes fuse to form the frontonasal process. The placodes deepen to form olfactory pits which lie between the medial and lateral nasal processes. The nasal septum will then grow posteriorly to divide the two nasal cavities. genital anomalies. About half of infants with choanal atresia display other abnormalities. This results in the persistence of a bony plate (90%). The newborn is a near-obligate nasal breather and the nasal obstruction will therefore produce difficulty in breathing. E. retarded growth and development. nose and paranasal sinuses all develop from the cranial portion of the primitive foregut. Embryology The mouth. Its persistence is thought to be the cause of choanal atresia. Older children may allow posterior rhinoscopy to view the occlusion. heart disease. It occurs in about 1 in 7000 births. G.CHOANAL ATRESIA Congenital choanal atresia is due to the embryological failure of the primitive bucconasal membrane to rupture before birth. membrane. colobama. Bilateral choanal atresia presents as an emergency at birth.

CHOANAL ATRESIA 33 Investigations The diagnosis can be confirmed by the mirror test or by attempting to pass a catheter through the nose into the nasopharynx. In the more common bony occlusions it will be necessary to perform a trephine and remove the obstruction with a burr or potassium titanyl phosphate (KTP) laser using the operating microscope. In the case of the newborn with bilateral atresia the first priority is to insert and maintain an oral airway. . Transpalatal. 1. The treatment of choanal atresia is surgical. This will not be possible if there is an obstruction. A stent should be inserted and a series of dilations of the choana will then be required to maintain an adequate lumen. Transnasal. Dilation will probably be necessary every 2 months initially. Fibreoptic endoscopy will confirm the diagnosis. but this period can be extended as the child grows. A CT scan is the method of choice to delineate the nature and thickness of the obstruction. If there is still doubt the lesion can be demonstrated radiologically. This is the usual approach in infants. particularly when the atresia is unilateral or if a previous transnasal opening has later closed. Two approaches are in common use. p. 2. The challenge is to provide a nasal airway which has an adequate mucosal lining. Follow-up and aftercare Maintenance of the opening following corrective surgery with regular bouginage is now mostly preferred to the use of indwelling tubes. A membranous occlusion may require no more than perforation with a probe. The soft palate is retracted. The palate is incised just in front of the posterior edge of the hard palate. 232. Related topic of interest Paediatric airway problems. and the occlusion removed together with part of the vomer and border of the hard palate. This can also be accomplished with electrocautery or laser. This is preferred by some surgeons. and to prevent granulation tissue formation and subsequent stenosis. Management Cases of unilateral atresia can initially be observed without treatment.

Congenital cholesteatoma has been shown by Michaels to be the result of the persistence of a small nidus of epidermoid ectoderm that occurs in the first trimester in the normal fetus and is normally resorbed. Although initially self-cleaning. but it can be divided into three groups with reference to the tympanic membrane. Therefore this skin is self-cleaning. (a) Primary acquired cholesteatoma associated with a defect in the pars flaccida. (a) The single most important fact about the skin of the eardrum is that in health it migrates from the centre of the drum outwards along the external ear canal. but unproven. Classification Cholesteatoma can be classified into congenital and acquired types. Put more simply. 1. It usually manifests itself as an anterior attic pearl behind an intact drum in the first year or so of life. carrying keratin and wax debris with it.J. (c) Tertiary acquired cholesteatoma exists behind an apparently normal eardrum as a result of implantation or previous middle-ear infection.CHOLESTEATOMA T. It may present later in childhood with extensive disease in an often cellular mastoid. 1. (b) Secondary acquired cholesteatoma associated with a defect in the pars tensa. resorbing underlying bone and tending to recur after removal. which in turn becomes infected and further expands under tension. Negative middle-ear pressure tends to pull the pars flaccida into the attic and may form a retraction pocket. Congenital cholesteatoma. As it expands the isthmus tends to narrow. compounding the problem and continuing the cycle. This is the most common.H. the epithelium eventually loses its capacity to migrate out of the pocket and is trapped. Primary acquired cholesteatoma. The incidence is approximately 10 cases per 100 000 per annum. The pocket fills with epithelial debris. There is no definitive classification of acquired cholesteatoma. These are distinct pathological entities. Aetiology There are a number of well-established. 2. it is ‘bad skin in the middle-ear cleft’.Lesser A cholesteatoma is a three-dimensional epidermal structure exhibiting independent growth. theories regarding the aetiology of cholesteatoma. . replacing middle-ear mucosa. Acquired cholesteatoma.

cholesteatoma is a benign keratinizing squamous cell cyst. but little is known as to how this growth is controlled. Microscopically. They are discussed under the topic complications of chronic suppurative otitis media (CSOM). but other changes in the surrounding perimatrix. probably accounts for some of the growth. Infection with bacteria causes an increase in clinical progression. The epithelial matrix of acquired cholesteatoma has approximately 15 layers whereas that of congenital cholesteatoma has only about five layers. lead to destruction of the bone locally. waxy deposit. or sensory.CHOLESTEATOMA 35 (b) Direct invasion of migrating squamous epithelium through the pars flaccida may occur. Electron microscopy shows normal epidermal cells plus Langerhan cells and Merkel cells. in turn surrounded by a matrix of inflamed subepithelial connective tissue. Initially the cyst of skin grows into the area of least resistance. (d) Metaplasia of middle-ear mucosa may occur secondary to episodes of chronic or recurrent acute otitis media. The principal signs are an attic crust. Marginal granulations and polyps protruding from the middle-ear cleft indicate osteitis and mucosal hyperplasia. (b) Acute otitis media may damage the fibrous layers of the pars tensa and a piece of squamous epithelium may be implanted should the tympanic membrane rupture. The drum may heal or there may be a permanent defect. Deafness may occur—conductive secondary to ossicular erosion. surrounded by an epithelium several cell layers thick. A positive fistula sign is said to indicate erosion into the labyrinth (see Labyrinthitis. respectively. Pathology Macroscopically there is a rounded pearly white mass of variable size. Clinical features Symptoms depend on the activity of the disease and arise either from the disease itself or from the complications. Complications may occur in acute exacerbation of the disease and are either within the temporal bone or intracranial. which may be scanty or just a flaky. Behind these may lie a cholesteatoma so that micro-otoscopic removal of an attic crust or aural polypectomy may allow the diagnosis to be made. In the centre are fully differentiated anucleate keratin squames. probably brought on by infection. The epithelium. but is often foul and creamy. A cholesteatoma invariably enlarges. Secondary and tertiary acquired cholesteatoma. 134). (a) Epithelium could migrate around the rim of a pars tensa perforation to cause a cholesteatoma. (c) Surgery involving trauma to the tympanic membrane (any middle-ear surgery or even grommet insertion) may occasionally allow squamous epithelium to be directly implanted. These changes include the activation of osteoclasts and the production of lysozymes. usually into the mastoid antrum and then into the air cells. The disease usually produces a discharge. being naturally migratory. probably from toxins involved in chronic inflammation migrating through the round window. often surrounded by friable granulations from infected bone or with polyp formation from infected mucosa. with skin going in rather than continuing out along the ear canal. Dizziness may indicate a labyrinthine fistula. a marginal perforation or a pocket of invading keratin debris. p. 2. . either as papillae through a temporary defect or merely as a change in the direction of migration in the upper part of the tympanic membrane.

including the ossicles. 159. (b) Pure tone audiometry (with masking). terminology and pathology of aural cholesteatoma. 18:245–255. T. 1998: 386–397. Further reading Ferlito A. Mastoidectomy. This usually takes the form of some type of mastoidectomy and tympanoplasty. Cholesteatoma surgery today.36 OTOLARYNGOLOGY Investigations (a) Micro-otoscopy (with the removal of attic crusts and polyps for reasons stated above). but the mainstay of treatment is surgical excision of the disease with reconstruction of the surgical defect and any conductive hearing loss. with sharply defined smooth margins. 1993. CT reveals a non-enhancing mass-eroding bone. (c) Radiology. A review of the definition. Angled otoscopes permit examination of the facial recess and sinus tympani. Related topics of interest Chronic suppurative otitis media—complications. Ludman and Wright (eds). London. In: Diseases of the Ear. In practice.341. p. it is often difficult on imaging to distinguish between cholesteatoma and pure mucosal disease.. Tympanoplasty. 42. Arnold. Palva. Youngs R. 107:483–488. isodense with CSF. Plain radiographs may indicate the height of the middle fossa dura and site of the sigmoid sinus but usually give little information on disease extent. Chronic suppurative otitis media—cholesteatoma. 1993. MRI likewise shows a mass with a low intensity T1 weighted signal and a high T2 signal. 6th edn. CT and MRI can both demonstrate the disease and give some idea of its extent. Journal of Laryngology and Otology. p. p. Clinics in Otolaryngology. Treatment Suction clearance may control early disease. If available. . examination with a rigid lens otoscope and otophotography should be performed.

swimming pool or sea water are the most common sources. Tinnitus. as is often quoted. The disease is described as quiescent during the first few weeks of a dry ear and inactive when the ear is dry long-term and active when a mucoid or mucopurulent discharge within the middle ear is present. often triggered by an upper respiratory tract infection. Most perforations arise when an acute perforation occurs during an episode of ASOM and. perhaps because of an inadequate dose. CSOM without cholesteatoma is sometimes referred to as mucosal chronic otitis media and subdivided into active and inactive. or via the ear canal when contaminated bath. The term ‘central’ implies there is a rim of tympanic membrane around the perforation and not that the perforation is centrally situated . This finding is also common with atticoantral disease. The patient may notice the hearing improves when the ear discharges indicating there is an ossicular discontinuity which has been bridged by mucopus or a polyp. the site. An air-bone gap of more than 30 dB is unusual and suggests an ossicular discontinuity. length or inappropriate choice of antibiotic. Tubotympanic CSOM The essential features are a central tympanic membrane perforation and adequate atticoantral drainage. Chronic mucoid discharge is associated with goblet cell hyper-plasia.CHRONIC SUPPURATIVE OTITIS MEDIA (CSOM) This can be sub-classified into tubotympanic or safe. A classification gaining more prominence is chronic otitis media with or without cholesteatoma. Clinical features Deafness is proportional to the size of the perforation and not. and tympanomastoid (atticoantral) or unsafe disease. typically momentary and initiated by sudden head movement are usually associated with a high tone sensorineural hearing loss secondary to toxins reaching the perilymph through the oval or round window. This allows sufficient time for squamous epithelium to migrate over the free edge of the tympanic layers to form a permanent perforation. there is slow resolution. the risk of serious complications is minimal. metaplasia of middle ear mucosa to respiratory type mucosa and poor mucociliary function. Disease is confined to the mucosa of the anteroinferior portion of the middle ear cleft. There is a 1–2% chance of developing a perforation when a ventilation tube is inserted and a 40% chance if a ventilation tube is in situ for more than 2 years. typically high pitched and vertigo. On examination there is a wet or dry central tympanic membrane perforation. Pathogens gain entry to the middle ear either via the eustachian tube.

the hearing in the contralateral ear. Typically mild and transient. High tone sensorineural hearing loss. An infected polyp may protrude through the perforation and there may be signs of the complications of tubotympanic disease. the frequency of recurrent infection. in contrast to the British National Formulary entry and the Committee on Safety of Medicines. Episodes can also be secondary to acute labyrinthine failure which usually reverses spontaneously but if a permanent paresis occurs it may take several months before compensation is complete. especially the long process of the incus. as the ear is at risk of serious complications. It has been suggested that some subjects are predisposed to the latter because of a narrow epitympanic space and indeed it has been shown by high definition CT scanning of the petrous temporal bone that as a group these subjects have a gap between the scutum and medial middle ear wall that is significantly narrower than in a matched group without CSOM. Ossicular erosion. sometimes causing florid granulation tissue formation. Intermittent benign paroxysmal positional vertigo has been described. Complications • • • • Otitis externa. Head and Neck Surgeons. Atticoantral CSOM Also called unsafe. until the ear is dry). • Middle ear adhesions. The former is attained by frequent aural toilet. age and general condition (see Tympanoplasty topic). prevent re-infection and to minimise the disability of any hearing loss. . is that the use of aminoglycoside antibiotics is reasonable in the presence of infection of the middle ear and a perforation (or grommet) for a limited period (i. Osteomyelitis of bone lining the polypoidal mucosa is the inevitable result. It is caused by either cholesteatoma or pure mucosal disease. further compromising drainage. the application of appropriate topical antibiotic ear drops.38 OTOLARYNGOLOGY in the tympanic membrane. The incidence of intracranial complications in atticoantral CSOM is the same for ears with cholesteatoma or with pure mucosal disease. In the event of an episode of AOM. The current view of the British Association of Otolaryngologists. eradicating any source of intercurrent or chronic upper aerodigestive tract infection and to prevent water entering the external ear canal when swimming or bathing. Intracranial and severe cochleovestibular symptoms are unusual as is a lower motor neurone facial palsy. the wish to swim and the patients occupation. Treatment The principles of treatment are to obtain a dry ear. The decision as to whether surgery in the form of a tympanoplasty or a hearing aid is more appropriate depends on the type and severity of the hearing loss. inadequate atticoantral drainage causes the mucosa to become chronically inflamed and polypoidal. • Tympanosclerosis. Vertigo. lifestyle.e.

CHRONIC SUPPURATIVE OTITIS 39 Clinical features Deafness may be a conductive. The BAO-HNS Newsletter. Facial nerve decompression is usually unnecessary. 1992. 1992. If cholesteatoma is not seen on examining the ear. Otoscopy may reveal no more than an attic crust which must be removed if cholesteatoma. in particular it does not distinguish between cholesteatoma. A high definition CT scan of the petrous temporal bone will show the extent but not the cause of soft tissue disease. The latter should cover anaerobes because they have been found in over 50% of cultures in children with CSOM. An unsafe ear without cholesteatoma which continues to discharge despite intensive medical management requires tympanomastoid surgery (see Mastoidectomy topic) as does the presence of cholesteatoma. lower motor neurone facial palsy. sensorineural or mixed. an attempt must be made to dry the ear by means of regular aural toilet. Pignatari SSN. American Journal of Otolaryngology. 1999. signs of meningitis or of raised intracranial pressure suggest a serious complication. . a unilateral headache. A marginal or attic perforation surrounded by granulation tissue or a polyp is more usual. the horizontal portion of the mastoid segment of the facial nerve was implicated as the site of involvement and the facial nerve palsy a neuropraxia which recovered with eradication of the cause. Burke P. CSOM. Pure tone audiometry varies from normal air conduction if there is limited attic disease to a severe mixed type of hearing loss in extensive disease. urgent surgery to irradicate all inflammatory disease is the priority. As with ASOM. Brook I. polypoidal disease or granulation tissue. smelly aural discharge. Exceptions to this rule may arise when the ear is the better or only hearing ear. Journal of Hospital Infection. 9:1. in very elderly or those medically unfit. Facial nerve paralysis secondary to chronic otitis media without cholesteatoma. Further reading Harker LA. 13:372–374. • Intracranial. A sanguinous discharge. perhaps because of florid granulations. In cases of lower motor neurone facial paralysis associated with CSOM. rarely responds rapidly to intravenous antibiotics because the mucosal changes or cholesteatoma are long-standing and surgical delay may compromise facial nerve recovery. 22 (suppl A): 75–87. serous and chronic otitis media: the role of anaerobic bacteria. Management The priority is to make the ear safe from intra cranial complications by eradicating disease. The former occurs when an ossicular discontinuity occurs from ossicular erosion by cholesteatoma or chronically inflamed mucosa. Scanty. mild transient vertigo and high pitched tinnitus are typical. Management of attic retraction pockets depends on their stage and in particular on whether they are self cleaning (see Cholesteatoma topic). otalgia. antibiotic ear-drops and systemic antibiotics. The management of acute. Complications • Extracranial. attic granulations or a perforation are to be revealed. unlike ASOM. Toxin penetration through the round window may be the mechanism of sensorineural loss.

Mastoidectomy. 35. Cholesteatoma. p. 159.40 OTOLARYNGOLOGY Related topics of interest Acute suppurative otitis media. . 5. p. p.

• • • • • • • • • Chronic otitis externa and meatal stenosis. the sinus confluence. Petrositis and Gradenigo’s syndrome (signs of ASOM. through osteomyelitic bone to reach the dura and lateral sinus or to affect a congenitally dehiscent facial nerve. (b) By retrograde propagation of small foci of thrombophlebitis which may extend through the temporal bone and dura to the major venous sinuses to cause a lateral sinus thrombosis and by further extension a cerebellar or temporal lobe abscess. Ossicular discontinuity from ossicular erosion. an ipsilateral abducent nerve palsy and pain in the distribution of the ipsilateral trigeminal nerve). Cholesteatoma. Classification 1. Middle ear adhesions. Squamous cell carcinoma of the middle ear. This may extend to involve the superior and inferior petrosal sinus. Lower motor neurone facial nerve palsy. Extracranial. Serous or purulent labyrinthitis. the superior sagittal sinus and the internal . Tympanosclerosis which may spread from the tympanic membrane over the ossicular chain causing ossicular chain fixation. the cavernous sinus.CHRONIC SUPPURATIVE OTITIS MEDIA— COMPLICATIONS Complications of CSOM are associated with a high morbidity and may be life threatening. 2. Intracranial. Labyrinthine fistula. • Lateral (transverse and sigmoid) sinus thrombosis. atticoantral mucosal disease and ASOM (see related topics) cause complications by spread of infection: (a) Directly via the oval or round window to reach the labyrinth. Browning in a retrospective study has calculated that the risk of a patient with CSOM developing an intracerebral abscess is 1 in 3500. (c) Along the periarteriolar spaces to cause a temporal or cerebellar lobe abscess.

• Extradural. and fast flowing blood no signal) and intracranial abscess (shows a centre of low attenuation with an outer rim of high signal). . A gadolinium enhanced magnetic resonance scan is now the investigation of choice for the diagnosis of an intracranial venous thrombosis (simple thrombus shows an intermediate signal. forgetfulness or drowsiness should have a full neurological examination looking in particular for signs of raised intracranial pressure. After confirmation some practitioners propose tying the internal jugular vein high up in the neck to prevent infective embolization during evacuation of infected clot. In this instance the palsy may be a neuropraxia of a dehiscent horizontal segment of the nerve. The diagnosis should be confirmed by needling the sinus. clumsiness. visual disturbance. Investigations A high definition CT scan of the petrous temporal bone will show the extent of mastoid disease although it may not distinguish cholesteatoma from mucosal disease. Clinical features Patients with acute intracranial complications usually present to the neurosurgeons and are most likely to be seen by an ENT surgeon after recovery from the acute episode. • Meningitis. If there is an actively discharging ear others would observe for at least 48 hours with the patient on intravenous antibiotics. A lateral sinus thrombosis if not responding to high dose intravenous antibiotics should have a cortical mastoidectomy and the lateral sinus exposed. There is often a concomitant extradural or subdural abscess which may have precipitated the formation of the thrombus. The lateral sinus is opened. A facial palsy secondary to ASOM is invariably a neuropraxia. subdural. meningitis and localizing cerebellar and temporo-parietal lobe signs. Patients with CSOM who present with unilateral or occipital headaches. found in 6% of ears. 1. 2. • Otitic hydrocephalus. vascularized thrombus. granulation tissue and slow flowing blood a high signal. The nerve does not require decompressing and should recover rapidly with aggressive treatment of the infection.42 OTOLARYNGOLOGY jugular vein. intracerebral (cerebellar and temporal lobe) abscess. the clot evacuated and the sinus obliterated with a temporalis muscle flap reinforced by a bismuth iodoform paraffin paste (BIPP) mastoid pack. vomiting. • Neurosurgeons to manage intracerebral abscess. The facial palsy in CSOM is usually secondary to compression from cholesteatoma or granulation tissue. A deep throbbing otalgia and serosanguinous discharge may herald malignant change. • Treatment of initiating otological disorder. Most otologists advocate an urgent mastoidectomy and decompression of the vertical segment of the facial nerve though this has recently been challenged. Subdural and extradural abscesses require a cortical mastoidectomy to provide adequate exposure before drainage. Treatment • High dose intravenous antibiotics to commence after taking a culture swab of the aural discharge.

Further reading Munz M. p. If a fistula is suspected from clinical signs and operative findings then either: 1) the matrix can be left over the affected portion of the labyrinth and a canal wall down procedure performed leaving an open cavity. Labyrithine fistulae may be caused by erosion of bone by cholesteatoma and by osteitis with the formation of granulation tissue. Auger L. Related topics of interest Chronic suppurative otitis media. Cholesteatoma. 2) the matrix can be peeled off under constant irrigation and the fistula immediately sealed with fascia or muscle as the final manouvre in surgery. 1997. 17:410–415. 38.5. Klester GR. Management of labyrinthine fistulae secondary to cholesteatoma. 1992. 21: 224–226. Farmer JP. or alternatively. Journal of Otolaryngology. Smith PG. Acute suppurative otitis media. p. et al Otitis media and CNS complications. Maxwell KS.CHRONIC SUPPURATIVE OTITIS MEDIA—COMPLICATIONS 43 3. . p. In cholesteatoma the matrix usually becomes apposed to the endosteum within the fistula and a protective walling off does not arise. 35. Herzog JA. American Journal of Otolaryngology.

There are two techniques in common use. It should be used when a tragal rub does not provide adequate masking. However. and in theory always when performing tuning fork tests. The maximum sound output varies from approximately 90 dB(A) when a box is held at right angles to the ear and 100 dB(A) when held over the ear. 1. exaggerated thresholds may be missed if suspicion is not aroused by clinical testing. but often only the Weber and Rinne tuning fork tests are performed. Masking Masking is as important in clinical testing as it is in audiometric testing. Proponents of clinical testing suggest that audiometry may be unnecessary if the hearing is normal or the results would not influence the management. audiometry on occasions may be inaccurate or unavailable. Furthermore. Clinical tests can be used to: • • • • Identify a hearing impairment. Bárány noise box. Determine the nature of a hearing loss (conductive or sensorineural). Occlusion of the auditory canal by putting finger pressure on the tragus with a rubbing motion is the easiest method. though this is not always practicable. . Detect feigning or a non-organic hearing loss. The tragal rub. but the main problem is cross-masking of the test ear. The non-test ear should always be masked when clinically testing by air conduction. This box produces a broad-band noise from a clockwork-driven source.CLINICAL ASSESSMENT OF HEARING Use of clinical tests It is surprising how often a clinical assessment of hearing is omitted from the routine examination of the otology patient. 2. Grade the severity. Voice tests and tuning fork tests are the two main methods. Using this technique speech will be attenuated by approximately 50 dB. These levels are sufficient to mask the non-test ear in all practical circumstances. There is a risk of under-masking if the sound level of speech arriving at the test ear is greater than 70 dB(A) so a Bárány noise box should be used when testing an ear with a severe or profound impairment or when testing bone conduction with tuning forks. The main reason that clinical tests of auditory function are overlooked is that they have largely been superseded by more sensitive and reliable audiometric tests.

The non-test ear is masked by a tragal rub unless a loud voice is required (use the Bárány noise box). to a loud voice at 60 cm. It can then be presented by either air or bone conduction. 2. In the presence of a purely conductive hearing loss. bluebell. which is the furthest away that is possible when masking the non-test ear. Tuning forks Tuning forks for audiological use are modified to include a finger grip on the stem and an expansion on the base of the stem to allow application to the skull. Forks with a frequency lower than 256 Hz can make it difficult for the patient to distinguish between hearing the sound and feeling it by vibration. to a whispered voice at 15 cm. 54. many of these tests are no longer in everyday use. For air conduction it should be held with its acoustic axis (a line joining two points near the tips of the two prongs) in line with and 2–3 cm from the external meatus. conversational voice and then loud voice at 60 cm and then 15 cm. numbers (e. A tuning fork should be set in vibration by a firm strike one-third of the way from the free end of the prong against a firm but elastic object (e. to a conversational voice at 60 cm.g. This should produce a relatively pure tone with minimal overtones. to a conversational voice at 15 cm. Ideally a 512. The easiest and best method of performing monaural free-field voice testing is by using a whispered voice. The sound level is increased in steps from a whispered voice at 60 cm. The tests are based on two main principles: 1. 4 B 7) can be used depending on the patient’s age and understanding. The inner ear is normally twice as sensitive to sound conducted by air as to that conducted by bone. A variety of tuning fork tests were developed to test absolute hearing thresholds (compared with the examiner). With the advent of newer and more sensitive forms of investigation. However. and finally to a loud voice at 15 cm. the pure tone thresholds are likely to be less than 30 dB (normal hearing).37. The duration of the stimulus decreases with increasing frequency. either mastoid process or vertex depending on the test. and cochlear from retrocochlear hearing loss. Patients who can hear a whisper at 15 cm or a conversational voice at 60 or 15 cm are likely to have thresholds in the range of 30–70 dB hearing level (HL) (mild/moderate impairment). It is usual to start by testing the better hearing ear when there is one. For bone conduction the base plate should be placed firmly on the skull. and it is difficult to activate forks with a frequency higher than 512 Hz sufficiently for them to be heard by those with a moderate or severe impairment. cowboy). the affected ear is subject to less environmental noise. The examiner starts using a whispered voice 60 cm away from the patient. Although the tuning fork can theoretically be placed at any point on the skull for bone conduction. If a patient can hear a whispered voice 60 cm away from the ear. . to differentiate real from feigned hearing loss. conductive from sensorineural.g. Those patients who can only hear a loud voice are likely to have thresholds greater than 70 dB HL (severe/profound impairment). The test finishes as soon as the patient repeats 50% of the words correctly at any one voice and distance level. making it more sensitive to bone-conducted sound. elbow or patella). some points may give less reliable results.CLINICAL ASSESSMENT OF HEARING 45 Voice tests Difficulties in standardizing the technique and variability of the stimulus provided by the examiner have led to criticisms of this test.or 256-Hz tuning fork should be used. Bisyllable words (e. a number of tests have stood the test of time and continue in current clinical practice.g.63) or combinations of numbers and letters (e. The patient is asked to repeat as accurately as possible what the examiner says.g.

In the normal subject or some subjects with a long-standing sensorineural hearing loss. First a tuning fork is placed 15 cm from the good ear. If a sensorineural hearing loss is present the sound will generally be heard in the normal ear. The tuning fork is struck and placed on the vertex. the sound should be heard in the affected ear. Unfortunately. A negative response (Rinne negative) will occur if there is a conductive loss of greater than 20 dB or if there is a severe sensorineural hearing loss. After the subject acknowledges hearing the sound. A positive response will also occur with a sensorineural hearing loss. the test is commenced by asking the subject to close his or her eyes to help concentrate on the sound. which has emanated into the external auditory canal. Bing test This test is similar to the Rinne and is based on the improvement in bone conduction perception in the normal subject when the external auditory meatus is occluded. Occluding the external auditory canal will block out ambient noise. The subject can be asked to compare either the loudness of the tuning fork when presented by air conduction and bone conduction (placed on the ipsilateral mastoid process) or the duration of the sound when presented by both air and bone conduction. if two pure tones of equal intensity are presented to both ears at once. the response is negative. The vertex is used as opposed to the forehead as the reliability of the test is thus improved from 72% to 86%. The tuning fork is struck and placed on the subject’s mastoid process. Weber test This test is based on the principle that a conductive loss causes a relative improvement in the ability to hear a bone-conducted sound and the test is of most value in a unilateral hearing loss. If the sound becomes louder. It can be performed in one of two ways. If the intensity of one side is increased. the sound will be heard in the midline. the sound will appear to originate in the midline. and usually indicates a conductive loss of 10 dB or more. the subject . the ipsilateral meatus is occluded by the examiner’s finger and the subject is asked if this makes the sound louder or quieter. The former is referred to as a true-negative Rinne and the latter as a false negative. (Further improvements can be achieved by using the upper incisors but these are not always available!) If a conductive loss of 10 dB or more exists.46 OTOLARYNGOLOGY No single test is diagnostic but all can provide useful information when taken in context. Stenger test This test is used to differentiate a real from a feigned hearing loss and is based on the principle that. from escaping. the sound will appear to originate from that side alone. In practice. minimally attenuated. in which case the false negative will become positive as the contralateral. If the sound does not change or becomes quieter. The normal response is to hear the sound as louder and longer with air conduction and is referred to as a Rinne positive. the response is positive (and normal). The two can be distinguished by using a Bárány sound box. The tester works behind the subject. bone conduction is masked. and prevent some of the bone conduction sound. Rinne test This test examines each ear individually and is again based on the principle of improved bone conduction perception with a conductive loss. tuning fork tests are unreliable in children.

Impedance audiometry p. Related topics of interest Examination of the ear. unknown to the subject. Non-organic hearing. two tuning forks are used simultaneously: one 5 cm from the bad ear and one 15 cm from the good ear. London: Butterworths. Pure tone audiometry. p. Speech audiometry. Stephens SDG. p. Report of the committee for the consideration of hearing tests. Clinical Otology and Audiology. 301. 1986. Unaware that there is a previously audible sound present at the good ear. 128. 4:421–430. Journal of Laryngology and Otology. Clinical Otolaryngology. If the hearing loss is real the subject will hear the sound in the good ear and report this. 82. Further reading Browning GG. 194. the subject will hear the sound loudest in the bad ear. . loss p. If the hearing loss is feigned.CLINICAL ASSESSMENT OF HEARING 47 confirms hearing the sound. 254. the subject will deny hearing anything and this suggests the diagnosis. A tuning fork is then positioned 5 cm from the bad ear. the subject will deny hearing it. 23–37. Finally. p. 48:22–48. 1979. Some tuning fork tests revisited. Committee for the consideration of hearing tests. 1933. Golabek W.

Evidence-based clinical practice.CLINICAL GOVERNANCE AND AUDIT Clinical governance In 1997 the government published the first of its white papers on quality within the NHS and introduced the term clinical governance. Risk management. Systems to ensure lessons learnt are implemented. community providers and primary care practices. Accreditation of hospitals. NHS organizations are presently NHS Trust Boards and the chief executive is ultimately accountable for assuring the quality of services provided by the Trust. research. Continuing professional development for all staff. to draw up and agree a development plan and clarify reporting arrangements. Developing guidelines and protocols. sharing of good practice and multidisciplinary team-work thrives. Development of clinical leadership skills. Managing the clinical performance of colleagues. A mechanism to ensure all systems are in place and functioning effectively. Clinical governance is defined as ‘A framework through which NHS organizations are accountable for continuously improving the quality of their services and safeguarding high standards of care by creating an environment in which excellence in clinical care will flourish’. to carry out a baseline assessment of capability and capacity. Health-needs assessment. Each health organization will be required to set up leadership and accountability arrangements. Continuing education for all clinical staff. developing guidelines and protocols. The systems embraced by clinical governance include: • • • • • • • • • • • • • Clinical audit. Audit of consumer feedback. . The third white paper—‘Clinical governance: Quality in the new NHS'—emphasizes the need for a move to a culture of learning in which education.

as reasonable targets and standards and this requires research. Audit Audit is defined as the systematic appraisal of the implementation and outcome of any process in the context of prescribed targets and standards. for each aspect of medicine. Being aware of best practice guidelines from NICE and adopting them as part of clinical audit or individual practice development. Determining methodology. Re-evaluating the quality of care. Taking a full part in continuing professional development programmes. and improve their practice. 2. 4. the most vital element being to ensure an improvement (indicating change) in care by reassessing results after the setting of criteria and standards. • It is educational and raises the overall quality of care. Clinical audit is the process by which medical staff collectively review. . 5. For individual practitioners these changes will mean: 1.CLINICAL GOVERNANCE AND AUDIT 49 New national bodies 1. the process and outcome of care and financial and administrative efficiency. 3. Working within the team to look at the strengths and weaknesses of the services they deliver and propose ways for improvement. 2. Leading and participating in quality improvement activities in service delivery. The reasons for performing audit are: • To encourage modification and improvement in clinical practice. Setting criteria and standards. 6. A working group of the World Health Organization defined audit as a 7-stage procedure. Setting priorities. evaluate. National Institute for Clinical Excellence (NICE) will set national standards and best practice guidelines. In the clinical setting the problem with this definition is what to define. • To allow peer review and support for clinicians. Playing a part in the organization’s assessment of its present capacity for quality improvement. The guidelines are: • • • • • • • Problem identification. Comparing performance with standards. Commission for Health Improvement (CHI) will inspect NHS organizations locally to ensure that clinical governance and the standards set by NICE are being implemented. Developing ways of involving users and carers in the planning of service improvements. This should include the assessment of patients access to care. Designing and implementing remedial action.

NCEPOD provides guidelines annually for specific clinical situations with the aim of improving surgical practice. district and even region has a relatively small number of clinicians performing a proportionately small number of procedures compared to the national total. with or without an anaesthetist. Audit on the other hand seeks to determine whether good practice (the process) has been adopted or whether the prescribed targets and standards gained through research are being met (the outcome). proposals made with the purpose of making them more efficient. relatives and their legal representative are allowed access to medical but not audit records. In other words audit tests either process or outcome after research has established that there is a link between them. Clinical research tests hypotheses so that they may be accepted as scientific fact or refuted in order to establish what is the best clinical practice. Hospital managers are allowed access only to the conclusions of any meeting. The guidelines are issued from information provided mainly by pathologists who supply data regarding perioperative deaths in their hospital. Important aspects of clinical audit are: • Clinical audit meetings should be confidential and involve only clinicians specifically involved in patient care. National Audit This is necessary because each hospital. • Treatment policies should be reviewed to minimize morbidity and mortality and maximize quality of life. . for example beds. A sample of the reported deaths are reviewed in greater detail by the steering group by sending questionnaires regarding all aspects of the patient’s care in the perioperative period to the consultant surgeon and anaesthetist in charge of the patient’s care. investigations. The recommendations come from an independent body with representatives across the surgical speciality fields (the steering group) nominated by an elected body in that speciality (in Otolaryngology it is a British Association of Otolaryngologists and Head and Neck Surgeons [BAO-HNS] proposed representative). The National Confidential Enquiry into Perioperative Deaths (NCEPOD) Perioperative deaths are those which occur within thirty days of a surgical procedure. In this context it should be remembered that patients. • Clinical audit regularly undertaken may provide a basis for a successful medico-legal defence because it can be shown that treatment has been researched and reviewed. • Each meeting should attempt to provide a specific recommendation which when implemented improves clinical practice. Anonymity of sensitive data must be secured. Type II errors in assessing clinical outcome might be averted. • Departments should set targets regarding appointments. investigations and duty theatres should be determined and if appropriate. involving local. that is any procedure carried out by a surgeon or gynaecologist. drugs. admission and outpatient waiting times. regional or general anaesthesia or sedation.50 OTOLARYNGOLOGY Research and audit Research and audit are often confused and it is important to clarify the difference. It allows prescribed targets and standards to be defined and may allow a management policy for a specific condition to be drafted. • The use of resources.

A First Class Service: Quality in the new NHS. Guidelines to Clinical Audit in Surgical Practice. The organization of quality assurance. Audit and research: complimentary but distinct. 1: 111–123.3807). The new NHS: modern and dependable. London: Department of Health. London: Department of Health. Clinical governance: Quality in the new NHS. London: The Stationary Office. Annals of the Royal College of Surgeons of England. Department of Health. 75:308–311. 1989. Quality assurance in health care. March 1989. 1993. . Bull AR. London: The Royal College of Surgeons of England. Department of Health. Department of Health.CLINICAL GOVERNANCE AND AUDIT 51 Further reading WHO Working Group. 1997 (Cm. 1998 (Health Service Circular: HSC (98) 113). 1999 (Health Service Circular: HSC (99) 065).

in effect procured central funding for cochlear implantation.COCHLEAR IMPLANTS S. The microphone unit is hooked behind the ear in a manner not dissimilar to a conventional behind-the-ear hearing aid. History The first report of cochlear implantation was from Djourno and colleagues in 1957 who described the insertion of a device into two totally deaf individuals. Implant design Current cochlear implants consist of two parts: an external component and a surgically implanted internal component. many individuals have derived greater benefit including the ability to understand speech with little or no lip-reading. the original premise that cochlear implantation would allow recognition of environmental sound and serve as an adjunct to lipreading has been realized. Not surprisingly.R. Michelson and colleagues in San Francisco. In appropriately selected individuals. but the MRC report by Summerfield and Marshall (1995) based on a multicentre pilot study. The external part comprises a microphone. Sound received by the microphone is converted into electrical energy. Clark and colleagues in Melbourne. many of the original and current commercially available devices bear their origins in these pioneering research programmes (3M and Clarion devices from California. Paralleled by developments in pacemaker technology. speech processor and transmitter coil. which is conveyed to the speech processor. USA. This body worn component utilizes various speech strategies (see below) and sends the processed signal to the transmitting coil which is held on the scalp behind the ear by a magnet in the coil and the implanted part of the device. USA. From the receiver-stimulator package. information is conveyed to the electrode array which is implanted within the cochlea: the current hypothesis . The transmitter coil transfers the processed information to the internal implanted receiver-stimulator package by transcutaneous induction. thereby stimulating residual auditory neural tissue. USA. Nucleus devices from Australia and Med-El devices from Austria). Initially.Saeed Over the last decade cochlear implantation has evolved to become an established means of auditory rehabilitation in selected adults and children with severe or profound hearing loss. Hochmair-Desoyer’s team in Austria and Chouard and colleagues in France. The device aims to provide perception of sound by attempting to emulate the transducer function of the cochlea. The success of these early implant programmes generated considerable interest in the UK: the first single channel device was implanted in London by Fraser in 1984 with the first multichannel device being inserted by Ramsden in Manchester in 1988. this stimulated considerable interest in the 1960s and 1970s among several investigators: the House group in Los Angeles. Australia. In reality. implant programmes in the UK were funded through research and charitable sources.

This information is presented in a pulsatile waveform to the individual channels of the electrode array. In addition. At the time of writing. There is no upper age limit as long as the potential recipient is in good health. hearing impaired individuals are classified as postlingual (speech acquired before becoming deaf) or prelingual (become deaf before acquiring speech). Depending on the manufacturer. The implementation of the principles of the speech strategies differs between manufacturers and continues to evolve. are unlikely to derive benefit from cochlear implantation as the neural plasticity required to make sense of the auditory stimulation from an implant has already been lost. Profoundly deaf prelingual adolescents and adults. Neural plasticity This is the ability of the central nervous system to be programmed to learn a task. In cochlear implantation two components are of paramount importance: changes in the brainstem auditory nuclei and the auditory cortex in response to sound and also the neural plasticity of speech articulation.and perilingual children the timing of cochlear implantation is critical taking into account the issues of neural plasticity.COCHLEAR IMPLANTS 53 is that the implanted electrodes stimulate the spiral ganglion cells of the auditory nerve directly. Current devices digitize the input and utilize band pass filters to divide the signal into frequency specific components. This reduces cross-interaction between channels thereby enhancing spectral information. Speech coding strategies A speech signal has two main components: spectral (pitch) information and temporal (loudness and change in loudness) information. Candidacy The process of selecting appropriate individuals for implantation is of critical importance for a successful outcome and is task that involves all the members of the implant team. the cost of the implant hardware in the UK is around £ 15 000. By stimulating a smaller number of the available electrodes with the signal components that have the highest amplitude the overall rate of stimulation increases. Auditory plasticity. A family history of longevity may also be taken into consideration. Modified electrode arrays are available for use in the partially ossified cochlea: compressed arrays carrying a smaller number of electrodes or double electrode arrays for insertion into the basal and middle cochlear turns independently. Age. The electrodes themselves are made of a platinum-iridium alloy housed in silicone with either a ceramic or silicone casing for the receiver package. In pre. The implanted component of the device needs to be constructed from biocompatible materials with high tensile strength and resistance to corrosion. In terms of outcomes. On this basis. the number of active electrodes varies from 12 to 24 (multichannel devices). a third group are those children that lose their hearing around the time of speech development (perilingual). however. The initial controversy surrounding implantation in children . enhancing temporal information. the current strategies for multichannel implantation from the different manufacturers are all capable of providing comparable results. is lost by the age of 8 years whilst the ability to develop good speech articulation only occurs if speech sounds are heard by the age of 3 years. Postlingual adults and children may be considered for implantation. and with it the ability to listen. The selection criteria continue to evolve and may be considered under the following headings: 1. The original strategies based on extracting vowel and fundamental formant information are now obsolete. Various speech coding strategies have evolved over the last 20 years in an attempt to emulate and present this information to the auditory nerve.

Loss of vestibular function may accompany the hearing loss. appropriate radiology gives information about the internal auditory meatus (the narrow meatus with normal facial function may only contain a facial nerve) and provides general information about the temporal bone anatomy such as pneumatization. Implantation is indicated in deafness due to cochlear pathology: central and auditory nerve causes are a contraindication. 3. particularly after meningitis. However. The principle of assessment of the patient’s general health prior to elective surgery under general anaesthesia applies as for any other planned otological surgery. different aetiologies have a greater or lesser effect on the spiral ganglion cell population. In addition. In children. autoimmune hearing loss and labyrinthitis due to causes other than meningitis. Imaging aims to firstly establish the presence of a normal cochlea (not always the case in congenital deafness) and to establish cochlear patency. soft tissue opacification of the tympanomastoid cleft and the anatomy of the jugular bulb. Surgery to render the ear disease free must be undertaken as a prelude to insertion of the device.54 OTOLARYNGOLOGY has abated and successful implantation has been undertaken in selected children below the age of I8 months. This is usually staged with obliteration and blind-sac closure of an open mastoid cavity if present. Duration of severe or profound deafness. With regards to children and adolescents. In the presence of cardiovascular or respiratory disease. Two imaging modalities are utilized. Central compensation occurs more readily in children than adults and the latter will require a caloric test to establish the presence or absence of labyrinthine function. 2. a decision has to be reached in terms of the risks of surgery against the benefits of implantation. The audiological evaluation includes aided and unaided pure tone audiometry and speech audiometry. the tympanomastoid cleft can be evaluated for the presence of any infection or cholesteatoma and surgery can proceed if the ear is disease free. In . with those individuals deafened for more than 20 years tending to fare less well. This may also be considered the case in deafness due to otosclerosis. At the time of implantation. 4. the severity of other disabilities such as blindness and locomotor dysfunction also require careful consideration. The standard examination is a high resolution CT scan. General medical history. Within the cochlea. CT scanning may fail to demonstrate cochlear fibrosis and therefore in post-meningitic deafness T2 weighted MR imaging is the investigation of choice. The original criteria for implantation were pure tone thresholds greater than 100 dBHL at 2 kHz and above with speech discrimination scores less than 10%. In postlingually deafened adults. Cause of the deafness. the relationship between the onset of deafness and speech development is of critical importance. In addition. Radiology may also demonstrate the aetiology in ‘idiopathic cases’ such as the large vestibular aqueduct syndrome or previously undiagnosed cochlear otosclerosis. More recently. with the observation that many implanted individuals seem to fare better than marginal hearing aid users several centres now use a 30% speech score as the ceiling for consideration for implantation. secondary changes in the cochlea such as fibrosis and ossification (such as after meningitis) need to be recognized as surgery may require a cochlear drill-out or use of a modified electrode array as described above. electrical response audiometry is utilized to confirm the presence of a profound hearing loss and to act as guide as to which ear to implant. Otological examination. particularly those with congenital deafness. the duration of severe or profound deafness is recognized as a prognostic indicator with respect to outcome. In addition. Audiometric and vestibular assessment Selected individuals that derive little or no benefit from a trial of conventional hearing aids may be considered for cochlear implantation. Radiological assessment. 7. Active chronic suppurative otitis media remains a contraindication to implantation. 6. 5. This is a mandatory part of the evaluation process. If implantation is to be undertaken in the ear with better or only vestibular function then appropriate preoperative counselling needs to be discussed with the patient.

The receiver package is then secured in its bed either with ties or bone cement. An attempt is made to initially preserve the endosteum of the scala tympani and to open into the basal turn with a needle rather than the drill. A cortical mastoidectomy with undermined margins is undertaken and a bed drilled in the skull for the receiver-stimulator package. clips or bone cement. Rehabilitation The initial ‘switch on’ of the device usually occurs after about 4 weeks when all the postoperative scalp swelling has settled and the wound is fully healed.COCHLEAR IMPLANTS 55 selected cases both types of imaging will be required in order to fully assess the feasibility of inserting the electrode array. An attempt is made to insert the array as far into the cochlear duct without damaging the array. Some surgeons prefer to enter the basal turn via the round window itself. The expectations of the potential adult recipient need to be realistic: the implant does not restore hearing in the natural sense and the patient needs to understand this. In addition the individual needs to be motivated for the intensive rehabilitation that will be required to maximize the potential from the device. rehabilitation requires numerous visits to the implant centre possibly over several years and the family need to commit themselves and the child to this process. thereby reducing the risk of trauma to the spiral lamina and remaining neural elements. The facial recess is approached via a posterior tympanotomy preserving a bridge of bone between the tympanotomy and the fossa incudis. The wound is closed in the conventional manner and a mastoid dressing and pressure bandage applied for 48 h. In children the expectations and motivation of the immediate family are also of critical importance. Two types of skin incision are commonly used: the extended endaural and modified post aural. The author routinely uses a facial nerve monitor and parenteral antibiotics are given at the start of surgery with two further doses postoperatively. an intensive programme of auditory and speech training takes place with fine tuning of the speech processing map for the particular individual. Psychological profile and expectations. The musculoperiosteal flap is usually raised separately. Surgery Surgery is usually undertaken under general anaesthesia after informed consent with particular reference to the facial nerve and chorda tympani. In particular. 8. . The tympanotomy should allow visualization of the incudostapedial joint and the round window niche to allow correct placement of the cochleotomy. For several weeks after this. A plain transorbital X-ray is undertaken the day after surgery to confirm the position of the electrode array in the cochlea. The full benefit of the implant is not usually realised for at least 6 months and may take 12–18 months when the learning curve flattens and the recipient adjust to the new auditory stimulus. A muscle plug is used to seal the cochleotomy and the posterior tympanotomy conferring further stability. The rehabilitation process continues for several months for adults and years for children. The proximal electrode array lies under the undermined margins and may also be secured with ties. The patient is usually fit for discharge on the third day post operation and the sutures removed at 1 week. The opening into the scala tympani is made just in front of and above the round window niche. The electrode array is guided into the cochlea and advanced using a claw designed for this purpose. In children considerable support from their teachers is required with close co-operation between the implant team and the educationalists.

therefore. Surgical complications. With experience and meticulous attention to incision placement and soft tissue handling major scalp complications can be avoided. Future developments Cochlear implantation is a fertile area for research and development both by implant teams and the manufacturers. Device malfunction is categorized as a soft failure if there is deviation from the specification without total loss of function (such as an electrode fault that can be programmed out) or as a hard failure if the implant ceases to function. Surgical complications in cochlear implantation are in fact relatively uncommon. The ultimate goal is the totally implantable device which is probably only a few years away. Current clinic studies include bilateral implantation. . This is probably because surgeons undertaking this type of work already have a considerable otological experience and international implant workshops are readily available for those embarking on this type of surgery. This situation is difficult to salvage and may result in device extrusion and subsequent need to remove the device. Complications 1. Injury to the facial nerve is rare whilst chorda tympani trauma is probably under-reported. cochlear implantation in patients with bilateral vestibular schwannomas and evaluation of music perception. the cumulative survival for devices from one of the manufacturers is greater than 98% after 5 years. Undesirable effects of electrical stimulation of the inner ear include pain in the ear. intrusive tinnitus and facial nerve stimulation. necessitating re-implantation. Such events have been reported by all the implant manufacturers and tend to occur early in the life of the device. All are uncommon and the offending electrode or electrodes can usually be programmed out. scalp or throat. Of the prelingually deafened children around one half developed open set listening with good or average speech intelligibility. Such tests assess the ability to distinguish speech without any contextual clues or lip reading. implantation in marginal hearing aid users. With continuing research and development device failure has become less common and by way of example. In one series almost all the postlingually deafened children developed open set listening with good speech intelligibility.56 OTOLARYNGOLOGY Outcomes Numerous tests have been developed to evaluate the outcome of implantation in a given individual. particularly when listening to familiar voices. The majority of adults report identification of environmental sound and a marked improvement in their lip reading skills. A sizeable proportion are able to track speech without lipreading and a smaller number can. open set tests are commonly used. Non-auditory stimulation. magnetless coupling mechanisms and refinements in speech processing strategies. Device complications. One of the most serious complications is ischaemia or sepsis in the scalp flap with loss of flap viability around the receiver package. Facial nerve stimulation is a particular feature in those individuals deafened by otosclerosis or temporal bone fractures and it is postulated that the fracture line or otospongiotic focus allows current escape and stimulation of the intralabyrinthine segment of the facial nerve. The outcomes in children are dependant on their language status at the time that the hearing was lost and to a degree on the age at implantation. to see children implanted at the age of 2 or 3 years entering mainstream education at the age of 5 or 6 years. 3. 2. Hardware developments include modiolus hugging electrode arrays. in ideal conditions converse almost normally or use the telephone. It is not surprising. In adults. Damage to the electrode array and electrode misplacement have been reported in most large series.

Cochlear implants. Oxford: ButterworthHeinemann. In: Booth JB (Ed). 1–25. 18 (Suppl6): 1–170. The American Journal of Otology. . 1997. Gibson WPR. Scott-Brown’s Otolaryngology. 1997.COCHLEAR IMPLANTS 57 Further reading Various authors. pp.

Refsum’s disease. 3. maxilla and mandible. 3. cerebellar ataxia. 2. Jervell and Lange-Nielson syndrome. There may be external. Hypoplasia of the malar bones. Recessive genes account for 80% of hereditary deafness. 5. Branchio-oto-renal syndrome. saddle nose. Waardenburg’s syndrome. There may be microtia or multiple. Most of these are non-syndromic and many are abiotrophies. Retinitis pigmentosa. external and inner ear abnormalities. glossoptosis. There are a multitude of syndromes associated with congenital deafness. craniostenosis and exophthalmos associated with external and middle ear abnormalities. cleft palate. maxillary hypoplasia. Hypoplastic mandible. Sensorineural hearing loss (SNHL) and a thyroid goitre. typically in late childhood in subjects with a previously normal cochlea in both structure and function (the abiotrophies). parrot beak nose. Telecanthus. middle or internal ear deformities. Usher’s syndrome. 2. Congenital fixation of the stapes footplate. Retinitis pigmentosa and SNHL. 5. pigment disorder (20% have a white forelock and 45% heterochromia iridis) with SNHL. Prolonged electrocardiographic Q-T interval and SNHL. Treacher-Collins syndrome. Crouzon’s disease.CONGENITAL HEARING DISORDERS We define the term congenital as existing at birth. renal dysplasia and a mixed type of hearing loss. cleft palate. Apert’s syndrome. . conductive or mixed and may occur in isolation or with other congenital abnormalities (the syndromes). Autosomal dominant 1. Hypoplastic mandible and maxilla. 4. Below are those we consider to be the most important: Autosomal recessive 1. Pendred’s syndrome. peripheral neuropathy and SNHL. Branchial arch anomalies. acrocephaly. Sensorineural deafness may be a hereditary degenerative deafness where there is progressive loss of hearing. Congenital deafness may be sensorineural. Pierre-Robin syndrome. syndactyly. 4.

Major aplasia. Major aplasia/atresia. hypoxia. The ventral arch cartilage forms the mandible (1st arch) and the hyoid bone (2nd arch). Perinatal disorders: e. syndromes associated with deafness. Ototoxic drugs (see ototoxicity chapter). 3. . Michel’s deformity. Bing-Siebenman dysplasia. 3. Mondini’s dysplasia. There are few hair cells and the saccule is collapsed.g. toxoplasmosis. They comprise: 1. congenital syphilis. especially in the high tones. Minor aplasia. Classification of congenital sensorineural deaf ness 1. Stapes surgery is difficult because of limited access and there is an increased risk of a perilymph gusher so that a small fenestra technique is recommended should stapedectomy be attempted. 2. Secondary to intrauterine disease (a) (b) (c) (d) Infections: rubella. usually of the stapes. cytomegalovirus. The bony labyrinth is normal. The external ear may be atretic. 4. These arches form the pinna (mesoderm and ectoderm). 2. (b) Deafness appearing in childhood: Deafness alone. Congenital conductive hearing loss The external ear canal develops from the first branchial cleft lying between the first and second branchial arches. The most severe ‘dysplasia’ (more correctly this is an aplasia) with agenesis of the labyrinth and total sensorineural deafness. The external and middle ear anomalies are classified into three groups: 1. mastoid pneumatization absent and there is a significant risk of one of the cochlear dyplasias. low birth weight. hyperbilirubinaemia.CONGENITAL HEARING DISORDERS 59 The dysplasias The dysplasias describe four congenital abnormalities of the cochlea and often occur as a component of the hearing syndromes. Hearing loss is severe. The stapes is usually functionally normal. Only the basal coil of the cochlea is present and the semicircular canals may be absent.g. hence its synonym cochleosaccular dysgenesis. Metabolic disorders: e. The external auditory meatus is narrow. the tympanic membrane functional. The bony labyrinth is normal. from the dorsal end of cartilage within each arch. but there is maldevelopment of the membranous labyrinth. premature delivery. bony labyrinth (mesoderm). 2. the tympanic cavity small. There is usually microtia with external ear canal atresia and fixation of an abnormal malleus and incus. maternal diabetes mellitus. syndromes associated with deafness. Anomalies of structures associated with these arches gives rise to multiple deformities. membranous labyrinth (ectoderm) and. Hereditary (a) Deafness present at birth: Deafness alone. for example Treacher-Collins and PierreRobin syndromes. Scheibe dysplasia. the ossicles (mesoderm). the pinna either normal or with a minor deformity and there may be ossicular fixation. but the stria vascularis has alternating regions of aplasia and hypoplasia. There are islands of residual hearing.

Pierre-Robin syndrome. Recent developments There have been significant advances in the genetic basis of hearing loss. . Management The congenital hearing loss may be suspected at birth because of the family history. depending on the cause. Waardenburg syndrome type 1 to the long arm of chromosome 2 and the branchio-oto-renal gene.60 OTOLARYNGOLOGY Classification of congenital conductive hearing loss 1. 3. Presently a safe. Fibrous dysplasia. Goldenhar’s syndrome. Mapping genes of non-syndromic deafness is difficult and relies on finding large families who have a significant number bearing the trait. Cystic fibrosis. Treacher-Collins syndrome. (a) Present at birth: e. and Tunnel DE. osteogenesis imperfecta. Further reading Lusting LR. non-mutated copy of a mutated gene coding for a deafness genotype has recently been shown to correct the phenotype so that when hair cell specific vectors are available. Sensorineural hearing loss in children. The introduction of a correct. Hereditary abnormal external or middle ear. Congenital disorders predisposing to glue ear. efficient vector to deliver the gene to a spiral ganglion hair cell and which produces long term transduction and a minimal immune response is still being researched. 2. Kartageners syndrome. Mutant genes coding for deafness at birth will be more difficult to resolve and will necessitate fetal gene therapy.g. These babies and those suspected of having one of the syndromes or dysplasias should be referred to a paediatric otologist or audiologist who will be able to investigate the suspected hearing loss and institute. Down’s syndrome. Mapping a gene gives rise to the possibility of gene transfer. otosclerosis. Many non-syndromic genes are now mapped as are several genes coding for syndromic deafness. cleft palate. 1998. Apert’s syndrome.g. appropriate surgery or/and rehabilitation. a homologue of the Drosophilia absent eye gene. The Jervell and Lange-Nielsen gene has been mapped to the short arm of chromosome 11. it may be possible to extend gene therapy to the abiotrophies. Crouzons disease. Easily identifiable regions of chromosomes (markers) are inherited and the ability to map a non-syndromic gene depends on the proximity of this gene to a marker so that the two are inherited together and in this way a linkage map is generated. 6:360–367. has been mapped to the long arm of chromosome 8. Current Opinion in Otolaryngology & Head and Neck Surgery. Congenital cholesteatoma. (b) Appearing in childhood: e. Miscellaneous conditions. Ideally the transgene insert will include an inducible promoter that will allow turning gene expression on and off according to need.

Related topics of interest Ototoxicity. 1999. Paediatric hearing assessment.CONGENITAL HEARING DISORDERS 61 Morrell RJ. Recent progress in hereditary hearing loss. p. 53. 228. p. p. 7:259–265. Cochlear implants. p. 117. Hearing aids. . 239. Current Opinion in Otolaryngology & Head and Neck Surgery.

sleep apnoea. under. facial reanimation. iliac crest (the bone here is cancellous) or a silastic implant will cover most situations. Functional: nasal obstruction. Technique Most rhinoplasty surgery consists of a basic technique comprising nasal dehumping. It is often the case that it is not possible to make an ugly nose pretty.or overprojected tip. so the patient will have a realistic expectation of the likely operative result. A dilemma in rhinoplasty surgery is what graft to use when augmentation is necessary. mid and lower thirds of the face. pinnaplasty. Much is written about the ideal nasal size and shape. Cosmetic: dorsal hump. In the USA there is a current vogue for external rhinoplasty which has the advantage of visualizing directly the osteocartilaginous vault during surgery. medial and lateral osteotomies with in-fracture and excision of a cephalic rim of lower lateral cartilage if the tip requires cephalic rotation. too wide or too narrow dorsum. . but it is usually possible to correct specific defects so that the nose no longer brings attention to the face. Cartilaginous augmentation by manoeuvring quadrate cartilage into a new position or using conchal cartilage with perichondrium attached. the thickness of the nasal skin and the race of the patient. It is important that the patient states specifically what they dislike about their nasal shape and for the surgeon to state exactly what deformities he is aiming to correct. bony dorsal augmentation using a rib graft (not a straight graft but it can be osteotomized). There is no singly perfect shape. The nasolabial angle should be about 90° in males and 110° in females. polly beak. snoring. hair transplantation and rhytidectomy. It is not disputed however that a nose should be straight and have a uniform dorsal width from nasion to the tip. Again there is no ideal graft that fits all scenarios.COSMETIC SURGERY This chapter is confined to a description of rhinoplasty. Rhinoplasty Indications 1. This however depends on the dimensions of the upper. 2. dorsal saddle.

The two common techniques are: 1. Anterior conchal scoring technique described by Stenstrom allowing the cartilage to curl back to form an antihelix without suturing. as the trauma to the ear from repeated redressing will predispose to infection or haematoma. slightly less satisfactory facial tone occurs. 2. thinning the region of the antihelix fold in the Mustarde technique with a diamond drill to reduce cartilage tension and to allow a more natural curve). Most surgeons will have their own modification of one of these techniques which works well for them (e.g. a cable graft using sural or great auricular nerve should be attempted. One year post onset is arbitrarily taken as the minimum time to allow the nerve to recover maximum function after injury or following attempted reinnervation. which usually indicates that a subperichondrial haematoma has formed due to inadequate pressure. Facial reanimation Surgery to produce improved facial symmetry after a facial nerve palsy should not be undertaken until the surgeon is sure there will be no spontaneous improvement. The only indication to remove the dressing is increasing aural pain. An important and often neglected portion of the procedure is the pressure dressing. Ideally.COSMETIC SURGERY 63 Pinnaplasty Most surgeons wait until the patient is at least 3-years-old so that the ear is not too small to manipulate and for the full deformity (e. The latter uses the larger branch to trapezius muscle with little loss of shoulder movement or strength. Reliable results are obtained only if anastomosis is attempted within one year of the onset of a palsy whereas the standard procedure is reliable when used up to two years after facial palsy.g. there may be an overlarge conchal bowl in addition to an absent antihelix) to become apparent. the operated ear being splinted and protected. It is unusual for the head dressing to be too tight and then the main symptom will be a persistent headache. Cotton wool should support the post-auricular region and fill the conchal bowl. This may be immediate if trauma. Otherwise. and a firm head dressing applied in such a way that it will not slip until it is removed 7–14 days later. has caused an immediate and total palsy suggesting nerve transection. When only half the width of the hypoglossal nerve is anastomosed to the facial trunk. in order to preserve tongue movement. For more proximal injuries such as those occurring after acoustic neuroma surgery. either external or iatrogenic. hypoglossal to facial or accessory to facial nerve anastomosis are the options. . Facial nerve grafting The reinnervation procedure chosen will depend on the site of injury and the surgeon’s personal preference. Mustarde technique in which the antihelix is folded and kept in position with mattress sutures. Many surgeons state that it is better not to apply a head dressing than apply one which is inadequate. surgery should be performed before infant school to prevent ridicule. Direct apposition of the nerve ending using monofilament 9–0 nylon suture material should be attempted only if it is possible to avoid tension on the anastomosis.

scalp expanders. They are placed into wounds created by needles or specifically designed small knife blades to create a 1 cm zone of single hair grafts. Up to 1000 grafts may be taken in a single session. The material is pre-stretched and so postoperative sagging is unusual in contradistinction to fascia lata. Rhytidectomy The original facelifts were the equivalent of modern minilifts in which an ellipse of skin is excised at or in the hairline and the tension of closure used to pull the facial skin taught. Male pattern alopecia is progressive and this may compromise long term results. micrograft. The material is attached to the zygomatic arch and the orbicularis muscle to elevate the mid-facial and perioral region. Most series have reported a high rate of extrusion and infection compared to fascia lata. which can occur early or several years after implanting. Eyelid procedures A gold weight implant positioned over the tarsal plate and centred at the junction of the medial and middle third of the upper eyelid has been used for more than thirty years to rehabilitate the eyelid following facial nerve paralysis. GoreTex being used when necessary to lengthen the sling. It can be compli mentary to facial nerve cable grafting or hypoglossal-facial anastomosis.64 OTOLARYNGOLOGY Dynamic and static suspension Dynamic suspension comprises transposition of the temporalis muscle to the submucosa or the orbicularis oris muscle in close proximity to the angle of the mouth. . The technique comprises placing the muscle sling lateral to the fascia overlying the muscles of facial expression to avoid the underlying facial nerve twigs. usually placed along the frontal hair line to give a natural feathered appearance. Implants of different weights are taped to the upper lid preoperatively to determine the correct weight to just allow closure without ptosis. or an incisional slit. A small percentage of patients who develop excessive alopecia including the fringe areas. scalp extenders and flaps now allow the creation of a virtually undetectable hairline and yield results not possible just five years ago. may not be suitable for any form of surgery. It improves the symmetry of the face at rest and on voluntary smiling in those with a permanent facial paralysis but does not improve lagophthalmos. Several sessions of mini and micrografts 3 or 4 months apart may be required to achieve a satisfactory result. In some centres only the middle section of the muscle is transposed. Micrografts are single hair grafts. Most patients with AA are candidates for some form of hair replacement procedure. Sterile 1 mm thick Gore-Tex Soft Tissue Patch can be used for static suspension in those unsuitable for dynamic suspension. The main complications are infection and haematoma in the early postoperative period and extrusion. Hair transplantation Modern techniques such as minigraft. To minimize extrusion rates it is recommended a drill hole is fashioned through the implant and this used to attach it to the tarsal plate by a nylon or prolene suture. Minigrafts (3–5 hairs per graft) are placed into holes created by a punch or laser. The commonest form of hair loss is androgenic alopecia (AA) which may present as male or female pattern AA or diffuse AA. Grafts are harvested from the dominant fringe using special multiblade knives which allow the harvesting of multiple strips of hair-bearing scalp simultaneously. The strips are then divided into micro or minigrafts.

In the 1970s a superficial muscle and aponeurotic system (SMAS) was described and most modern facelifts involve elevating the SMAS and fat to provide a more effective and longer lasting result. 1992. Quast LM. Scamp T. deep plane facelift and the composite and extended SMAS facelift. allowing elevation up to the midline. 92. Temporalis muscle for facial reanimation: A 13-year experience with 224 procedures. Facial nerve palsy. Rhytidectomy: past. Hypoglossal-facial nerve anastomosis. Drucker C. p. Ebersold MJ. the details of which may be found in operative texts. 119:378–382. . The technique has been further developed to the present day multi-directional facelift. Morbidity after gold weight insertion into the upper eyelid in facial palsy. O-Uchi. 77:51–54. Journal of Neurosurgery. 267. Archives of Otolaryngology Head and Neck Surgery. British Journal of Plastic Surgery. May M. Reconstructive surgery. Current Opinion in Otolaryngology and Head and Neck Surgery. 1997. Long-term results of spinal accessory nerve-facial nerve anastomosis. 487: 80–84. Further reading Kunihiro T. Acta Otolaryngologica. 1993. Kanzaki J. subperiosteal facelift. 177. present and future. This technique had the disadvantage of occasionally causing skin necrosis or a wide scar due to increased skin tension on the suture line. p. 5:234–242. 1992. Campbell AC and Shumrick KA. Related topics of interest Nasal trauma. p.COSMETIC SURGERY 65 Anterior subcutaneous elevation in a plane superficial to the fascia of the muscles of facial expression to avoid injuring the facial nerve became widespread in the 1970s. Harrison DH. Pickford MA. 1991. 45:460–464.

theatres and recovery area. Patient selection The patient may be admitted into either a self-contained day surgery unit with its own admission suites.DAY CASE ENT SURGERY Definition An ENT surgical day case patient is one admitted for operation on a planned non-resident basis but who requires facilities for recovery. and patients should normally be of ASA I or ASA II status (the American Society of Anesthesiologists classification of physical status: class 1. Operations likely to take longer than 60 min are unsuitable because of the slow speed of recovery from general anaesthetic. for example after adenoidectomy or submucosal diathermy. for example non-insulin-dependent diabetes mellitus or essential hypertension). and legal documents should not be signed during the first 24-h postoperative period. The patient must be taken home by an adult in a car or taxi on discharge. physiological. when alcohol is also forbidden. An example of a guideline sheet is shown in appendix 1 and can be modified according to the preferences of each unit. As a rule an upper age limit of 75 is recommended although older patients with a low biological age should be considered. mild-to-moderate systemic disturbance caused either by the condition to be treated surgically or other pathophysiological processes. An adult must be available to supervise the patient during the evening and first night. wards. or class 2. the patient has no organic. . A telephone must be accessible so that the hospital can be contacted in an emergency. or less desirably a day case ward or unsatisfactorily a general ward. No mechanical device should be used nor cooking undertaken. In a general ward booked admissions may be blocked by emergency admissions. Full admission procedures and records are required. Patients with a body mass index (BMI) greater than 35 are unsuitable. this is an expensive option because the ward is not closed at night or at the weekend. The home should be within a 20-min drive of the hospital if the patient is at risk of a primary haemorrhage. which therefore excludes those operations and procedures undertaken in the outpatient or accident and emergency department. Driving is not advised within 48 h of a general anaesthetic. guidelines for surgeons regarding medical suitability for day case surgery. by collaboration between anaesthetists and physicians. Every day surgery unit should produce. biochemical or psychiatric disturbance and the pathological process for which surgery is to be performed is localized.

Early mobilization. • In-patient admission. skin tags. Increased efficiency. Excision of accessory auricles. preauricular sinuses. bilateral antral puncture. for example vocal cord polypectomy or nodule excision and laser excision of small tongue lesions. Advantages • • • • • • • Lower costs. 2. They should have their own designated area away from adult patients. septoplasty. A preadmission visit allows familiarization. Other indications include the division of tongue tie and lymph node excision biopsy. electrocautery of the nasal septum. limited intranasal polypectomy. Ear. Revised edition.DAY CASE ENT SURGERY 67 Paediatric surgery Special facilities for children are required. Adenoidectomy. myringotomy with or without grommet insertion. Less psychological preparation required. aural polypectomy. It is permissible to have a children-only operation day in a day surgery unit or day case ward if the required facilities are present. limited functional endoscopic sinus surgery. tonsillectomy (controversial). Reduced in-patient theatre workload. sub-mucosal diathermy of the inferior turbinate. Nose. if needed. must be arranged at short notice. . Wedge excision biopsy of pinna lesion. Surgery time should be less than 1 h. Reduction of nasal fractures. Appendix 1 Selection criteria All patients should be ASA I or II and ambulant. London: The Royal College of Surgeons of England. Disadvantages • Limited care available to the patient after discharge. submucosal resection of the nasal septum. with its own play area and parental waiting area. Appropriate Procedures 1. Anaesthetic administered allows rapid recovery. Reduced disruption to life. examination under anaesthetic (EUA) and biopsy of the laryngopharynx and oesophagus provided there is no risk to the airway. Selected patients requiring laser therapy. 3. Further reading Report of the Working Party on Guidelines for Daycase Surgery. 1992. Removal of impacted wax or foreign bodies. Head and neck. The children’s area should be staffed by paediatric-trained nurses.

nausea or very slow to arouse) Social circumstance Unsuitable Suitable Unsuitable Unsuitable Suitable Suitable Unsuitable Suitable Unsuitable Suitable Unsuitable Unsuitable Suitable but instruct no medication on day of surgery Unsuitable Suitable Unsuitable Suitable Suitable Unsuitable Refer for assessment Suitable Refer for assessment Suitable .g. ECG satisfactory <12months CVS MI less than 3 years ago Unstable angina Symptomatic heart disease Ventricular arrhythmia Pacemaker due to 2nd or 3rd degree heart block Stable angina or controlled atrial fibrillation with satisfactory ECG and serum urea and electrolytes Hypertension BP < 170/100 BP > 175/105 Respiratory disease COAD or emphysema but: (i) able to climb two flights of stairs (ii) unable to climb two flights of stairs Asthma Well controlled on inhalers Previously hospitalized or taking systemic steroids Diabetes Insulin dependant NIDDM and BM stix < 11 and ECG satisfactory Neurological disease Restriction of normal activity or CVA within past 1 year Not restricting normal activity Epilepsy Poorly controlled Well controlled (no seizures during previous 1 year) Hiatus hernia Consider H2 blockers before surgery Bleeding disorder Drug history Systemic steroids within previous 3 months or cardiac drugs other than antihypertensives or taking MAO drugs Diuretics but satisfactory ECG and serum urea and electrolytes Anaesthetic problem Difficult intubation Malignant hyperpyrexia ITU admission Blood relative died or had any of above Minor (e.68 OTOLARYNGOLOGY No escort home No adult overnight Lives > 1 h away Age 60–75 years but fit.

but this is not invariable. Epiglottitis is usually seen in children between the ages of 2 and 6 years. Initially the child usually complains of a sore throat and pain when swallowing. There seems to have been a decline in new cases over the last few years. flushed appearance and a high temperature (38–40°C). but predominantly the loose connective tissue of the epiglottis.EPIGLOTTITIS Acute epiglottitis is an uncommon but dangerous bacterial infection of the throat. A critically ill. Attempts to depress the tongue or indirect laryngoscopy should not be undertaken to confirm the diagnosis as this can precipitate laryngospasm. Clinical features The disease may present at any time of the year but is more common in winter. especially in adult cases. Haemolytic streptococci. Inspiratory stridor then occurs. Prophylaxis In recent years efforts have been focused on the prevention of HIB infections. It has been suggested that previous contact with H. . This can also occur if the child becomes distressed and starts to cry. It may also occur in adults. The inflammation and oedema will rapidly progress to cause muffling of the voice and respiratory obstruction. influenzae in early childhood may later be followed by a type III Arthus hypersensitivity reaction which would account for the rapid onset of epiglottitis. The child will usually sit up and lean forward dribbling saliva. In children under the age of 2 years Haemophilus tends to cause meningitis. so nothing that may be frightening should be allowed. Aetiology Haemophilus influenzae type B (HIB) is the usual causative organism. Quite why the infection has a predilection for the epiglottis is not clear. There is an acute inflammation of the larynx which affects all the supraglottis. pneumococci and staphylococci have also been isolated. breathless child may then present to the casualty department having a toxic. The provisional diagnosis is made on the history and the examination of the child. which may be attributed to the new conjugated HIB vaccine approved for administration to 2-month-old infants. with a peak incidence between the ages of 3 and 4.

The child is allowed to remain in an upright posture as sudden changes in position. and if intubation fails a rigid bronchoscope should be inserted immediately and subsequently replaced with an endotracheal tube. 2nd edn. and all investigations should be delayed until this is secure. This should then be replaced with a nasotracheal tube as they are more readily tolerated and more securely fixed. Childhood epiglottitis in recent years. 25:155–162. The oxygen saturation is closely monitored with pulse oximetry. An intravenous line is inserted for fluid replacement and antibiotic therapy. no child should be sent for a radiograph without the continuous presence of someone skilled in paediatric intubation. An appropriately sized orotracheal tube is inserted to immediately restore the airway. The taking of a radiograph should never be done if epiglottitis is suspected and there are already signs of respiratory difficulty. epidemiology and outcome in a population before large scale Haemophilus influenzae type b vaccination.70 OTOLARYNGOLOGY Investigations Maintenance of the patient’s airway is the primary consideration. 1989. Oedematous aryepiglottic folds and a cherry red epiglottis are characteristic signs of the disease. Some surgeons advocate the use of corticosteriods before decannulation to help reduce oedema caused by the tube. A parent should be present and at all times the child is talked to and reassured. The current choice of antibiotic is chloramphenicol (100 mg per kg body weight per 24 hours) as up to 30% of Haemophilus strains are resistant to ampicillin. Westmore RF. There may be difficulty establishing an endotracheal airway. Paediatric intensive care. Acute epiglottitis—aetiology. the parent is shown from the room. The sedated child is transferred to a paediatric intensive care unit for rehydration. In the early case a lateral soft-tissue neck radiograph may confirm a swollen epiglottis but is not essential and may be dangerous. Marsh R. et al. Pascucci RC. International Journal of Otolaryngology. Direct laryngoscopy should be performed to establish the diagnosis and to pass an endotracheal tube.) Paediatric Anaesthesia. 1327–1337. 19:441–445. Once the child is afebrile and appears well. antibiotics and humidified inspired gases. extubation can be considered. An experienced paediatric anaesthetist and otolaryngologist should be in attendance. A nasogastric tube should be inserted for feeding. may result in airway obstruction. third generation cephalosporins are an alternative. Rarely. As the epiglottic oedema settles an increasing leak around the endotracheal tube is expected. . especially lying down. Further reading Hugosson S. Follow-up and aftercare There is usually a prompt response to treatment with fluid replacement and antibiotics. Furthermore. In: Gregory GA (ed. 1994. When the child is asleep. A gentle inhalation induction using sevoflurane and oxygen is preferred. New York: Churchill Livingstone. a tracheostomy may be necessary. Because of the side effects of chloramphenicol. This is usually possible within 48 hours. Once an airway has been established swabs are taken from the epiglottis and a blood culture is performed. Intravenous access is not attempted and the child should be moved to a quiet induction area with adjacent operating facilities. Clinical Otolaryngology. 1993. Kessler A. Treatment The first requirement of treatment is to safeguard the airway.

EPIGLOTTITIS 71 Related topics of interest Paediatric airway problems. p. 237. . Paediatric endoscopy. 232. p.

Inflammatory (rhinitis. Little’s area (Kiesselbach’s plexus) is the commonest site of bleeding. Traumatic (fractures. nose picking). Clinical assessment Always make sure that the patient is not in shock. pregnancy). sinusitis). superior labial). foreign body. Raised venous pressure (whooping cough. latrogenic (surgery. Neoplastic (tumours of the nose. General causes • • • • • Anticoagulants (warfarin. which may be more to do with its comparatively exposed position in the anterior part of the septum than the fact that this is where the vessels anastamose. Diseases of the blood (haemophilia. Blood vessels involved The upper parts of the nose are supplied by branches from the internal carotid artery (anterior and posterior ethmoidal arteries) and the rest from branches of the external carotid artery (greater palatine. but the instigation of immediate resuscitation is not usually necessary. Endocrine (menstruation. . It is important that nursing support is available in this situation to assist with management of the patient. pneumonia). Hypertension. Familial haemorrhagic telangiectasia (Osler-Rendu-Weber). Local causes • • • • • • • Idiopathic (85%). sphenopalatine. leukaemia). 2.EPISTAXIS Aetiology 1. steroid nasal sprays). especially when bleeding is brisk. Protect the patient’s clothing and your own with an apron. sinuses and nasopharynx). air conditioning). Environmental (high altitude. aspirin).

A Caldwell Luc incision is made. The bleeding is usually stopped by one of the following methods: • • • • Pressure on the nostrils (can be supplemented with ice-cold packs and sucking ice cubes). merocel). above the middle turbinate. Management The aims are to arrest the haemorrhage and to treat the underlying cause. Hereditary haemorrhagic telangiectasia A specific problem in the management of epistaxis (and favourite examination topic) includes hereditary haemorrhagic telangiectasia or Rendu-Osler-Weber disease. Anterior ethmoid artery dipping is required for uncontrollable bleeding from the upper part of the nose. Foley’s catheter. Brighton balloon). as well as telangiectases on . cerebrovascular embolus) has not been fully accepted. Investigations should include a full blood count (FBC) (check Hb. The approach to the anterior ethmoidal artery is via a medial orbital incision with lateral displacement of the upper orbital contents. If the bleeding has been significant start an intravenous infusion. Local cautery (chemical or electrocoagulation). The artery is surrounded by periosteum about 2. Surgical intervention 1. 4. Further surgery is indicated only on the rare occasion when haemorrhage is not controlled by packing and cautery.EPISTAXIS 73 and wear gloves. Anterior nasal packing (paraffin gauze. clotting studies and blood for group and cross-match if necessary. Endoscopic approach. Ligation or dipping of the maxillary artery in the pterygomaxillary fossa. External carotid artery ligation Ligation of the external carotid in the neck may be needed if maxillary artery clipping is unsuccessful. 6.v. If nasal packing is required. especially the tongue. and sinusitis. Examination under general anaesthetic may become necessary if the above measures fail to allow better identification of the bleeding site and more effective cautery and packing. Embolization of vessels under radiographic control with gel sponge or beads is advocated in some centres. or if a severe epistaxis recurs. Submucosal resection 2. BIPP. The artery is encountered in the pterygopalatine fossa and teased away from the fat pad. For exposure and ligation of the sphenopalatine artery. Calm reassurance coupled with sedation (i. Patients with this are easily recognized by red spots on the lips and the mucous membrane of the mouth. 5. the antrum entered and a window made in the posterior wall of the sinus. 3. white cell count and platelets). systemic antibiotics should be given to prevent otitis media from Eustachian tube blockage. diazepam) will relieve the patient’s anxiety.5 cm deep to the orbital rim just above the level of the medial canthus and is readily controlled by clipping. Packing of the postnasal space (gauze. Each tortuous branch is clipped in turn. but because of the risks involved (e.g. Take a full history and on examination try to localize the area from which bleeding is arising and any specific bleeding points.

p. Related topic of interest Examination of the nose. The condition may be complicated by the presence of lesions in the gut. Clinical Otolaryngology. but all patients who have required admission and treatment in hospital should be reviewed in the outpatient department. Endoscopic ligation of the sphenopalatine artery. radiotherapy. The patient is asked if there has been any further bleeding and their haemoglobin levels checked before discharge. which may bleed. In addition to repeated local treatment. or arteriovenous malformations in the lungs. 84.74 OTOLARYNGOLOGY the face and nose. . Follow-up and aftercare This depends on the cause and severity of the bleeding. lining mucosa with placenta or split skin grafts and laser therapy (argon or Nd-YAG). Further reading McGarry. other therapies include oestrogens. sclerosants.

. leading to a behavioural change in those required to follow a different way of working.J. and reaching a conclusion about which option would have the greatest liklehood of effectiveness’. to assess the research evidence. incentives that are locally negotiated and agreed are more likely to succeed than those imposed from above. performance feedback and empowerment have all been shown to be effective but need resourcing. as well as taking note of systemic reviews that have been performed by institutions such as the Cochrane Centre and through the medium of well drawn-up guidelines. The first two points concern the equipping of clinicans and managers with critical appraisal skills. difficulties in developing evidence-based clinical policy. and training. Problems There are many reasons cited for the reluctance to embrace EBM into daily clinical practice: 1 . 3 . Apart from the barriers identified. finding and evaluating all relevant research evidence.Bradley Definition The term ‘evidence based medicine’ (EBM) was first used in the 1980s at McMaster University in Canada. During the 1990s it was defined as: ‘medical practice in which clinical problems are addressed by formulating clearly defined questions. Poor compliance to treatments by patients. A veriety of interventions are required. there is also the need for changes in clinical behaviour that are necessary to ensure the successful implementation of guidelines. A change in behaviour can be reinforced by providing incentives to work in a different way. difficulties in applying evidence due to: • • • • • poor access to best evidence and the need for validated guidelines. The heterogeneity of the patient population. Incentives such as financial reward. patients and employers. poor continuing educational programmes. education.EVIDENCE BASED MEDICINE P. Access to evidence is improving with the recognition for the need of a ‘chief knowledge officer’ to dissemninate information to the rest of the organization. 2 . As with the pocess of obtaining the commitment of stakeholders. the size and complexity of the research required. organizational barriers. resource allocation.

1. with level la being evidence obtained from meta-analysis of randomized controlled trials (the gold standard) to level 4 which is the evidence obtained from expert committee reports or opinions and/or clinical experience of respected authorities. The best available clinical evidence refers to clinically relevant research.76 OTOLARYNGOLOGY Clinical governance The introduction of Clinical Governance with the expectation that the use of guidelines and audit will improve patient care. Clinical evidence EBM is the conscientious. EBM divides clinical questions into a number of types. the steps in answering them are the same. Regardless of the type of question asked. • Prognosis questions—outcomes. EBM is simply a method for identifying and interpreting the relevant research data to help with the questions faced in our clinical lives. • Treatment questions—ask what the efficacy of a specific treatment is commonly compared to placebo. being able to appraise the evidence we find for validity and usefulness. and the efficacy and safety of therapeutic. Interpretation In essence. The National Services Frameworks will rationalize this process in the UK through the National Institute for Clinical Excellence (NICE) with external monitoring being provided by the Commission for Health Improvement (CHI). with no direct comparison of treatments. applying the evidence to pure practice. EBM includes audit as well as consideration of the external evidence. Its practise requires the integration of individual clinical expertise with the best available clinical evidence from systematic research. rehabilative and preventa-tive regimens. therefore. • Diagnostic test questions—the accuracy of diagnostic or prognostic tests. The levels of evidence are classified as 1–4. • Harm and aetiology questions—the risk of harm arising out of treatments or interventions or about the association between a factor and a medical condition (smoking and lung cancer). What is the evidence? . evaluating our own resulting performance. efficiently tracking down the best evidence with which to answer them. The BAO-HNS will work with these groups and will welcome the additional contribution being made by the National Otolaryngological Trials Office (NOTO) in Newcastle and by the Cochrane ENT Working Group in Oxford. The feedback loop implied by the last two points indicates the relationship between audit and EBM. explicit and judicious use of current evidence in making decisions about the care of individual patients. which may be from basic sciences. The steps comprise: • • • • • rephrasing our problems or information needs into answerable questions. but in particular from patient centred research into the accuracy and precision of diagnostic tests. the power of prognostic factors.

Edinburgh: Churchill Livingstone. There are several reasons for not performing RCTs in surgery. Conclusion A review of the published literature during 1990–1994 in five major general otolaryngological journals. Moloney NC. Which clinical studies provide the best evidence? British Medical Journal 2000. Haynes B. 1:27–34. the benefits of the treatment are so great and obvious that such a trial would be clearly unethical. Medical management of appendicitis against surgical appendicectomy. Stewart-Brown SL. This situation is not confined only to surgery: old drugs such as morphine. Clinical Otolaryngology. Maran AGD. 22:483–484. What are general practitioners’ attitudes towards evidence-based medicine. The second obstacle to trials of operations is the difficulty that arises when attempting to compare surgical against non-surgical treatments. Evidence-based medicine: how to practise and teach EBM. 1997. suggested that there is poor evidence base for our specialty if one regards randomized controlled trials as the gold standard. Once a treatment is accepted as the standard for the management of a given condition. 1997. Richardson WS.EVIDENCE BASED MEDICINE 77 2. particularly their failure to conduct randomized control trials (RCTs). 22:152–157. 1997. Evidence medicine: a new approach to teaching the practice of medicine. 1999. Evidence-Based Medicine Working Group. 317: 273–276. Barriers and bridges to evidence based clinical practice. In many cases. Should we change our practice because of the new evidence. Is the evidence important? 4. there are important practical difficulties in performing RCTs of surgical operations that do not exist with most medical treatments. It is difficult to blind patients and staff to the operation performed. Is there evidence base for the practice of ENT surgery? Clinical Otolaryngology. Rosenberg W. and are these changing? Journal of Clinical Excellence. High quality observational studies may extend evidence over a wider population and are likely to be dominant in the identification of harms and when randomized controlled trials would be unethical or impractical. JAMA. 1992. Is the evidence valid? 3. though this can sometimes be done with an imaginative trial protocol. 1998. If so how? Problems Surgeons have been severely criticized for their failure to apply EBM in the past. Finally. Ah-See K. one UK and the other four USA based. Barton S. 268:2420–2425. Haynes RB. First history. Studies more recently do not justify a major revision of the hierarchy of evidence. . Further reading Patterson JV. it is difficult to achieve the level of uncertainty (‘equipoise’) about its benefit required to persuade clinicians to test it again against a placebo. Armstrong MWJ. Clinical guidelines for otorhinolaryngology. British Medical Journal. but they do support a flexible approach in which a randomized controlled trials and observational studies have complementary roles. Haines A. Bradley PJ. Sackett DL. asprin and digoxin are also difficult to randomise against a placebo. 321:255–256.

The active electrode is usually a trans-tympanic needle placed on the promontory (canal electrodes may be used but give a less satisfactory signal) after preparation with local anaesthetic. It is diphasic at threshold and has a signal latency which decreases with increasing signal intensity and is made up of three parts: 1.EVOKED RESPONSE AUDIOMETRY In response to sound stimulation. • Cortical electrical response. The test signal can be produced using a loudspeaker or headphones (especially if acoustic conditions are less than ideal). Physiology The signal recorded by ECochG is described as a compound action potential. A ground electrode is attached to the patient’s forehead and a reference electrode to the ipsilateral mastoid. . so the tests are less open to the bias in results which arise in those tests requiring patient cooperation. However. the tests are not truly objective as a tester will have to interpret the complex tracings obtained from the procedure. No conscious response is required from the patient. It has no threshold and increases in amplitude with the stimulus intensity. Evoked response audiometry (also called electric response audiometry) is a technique designed to measure these signals. As the amplitude of the evoked electrical response is small relative to the body’s background electrical noise. a variety of filters and an averaging computer are used. Its polarity follows that of the test signal. The cochlear microphonic. • Brainstem electrical response. Electrocochleography Electrocochleography (ECochG) aims to measure the signal produced by the cochlea and cochlear nerve in response to acoustic stimulation. Technique The patient lies comfortably in a soundproof room. This signal is produced by the hair cells and resembles the pattern of the basilar membrane vibration. Wideband clicks and high-frequency tone bursts are the usual stimulating test signals. electrical signals are produced by various parts of the auditory system from cochlea to cortex. In practical terms three main responses can be recorded: • Electrocochleogram.

The hardware and test signals used (wideband clicks and high-frequency tone bursts) are identical to those used for EcochG. 2. because of their size. several thousand responses are analysed as opposed to hundreds in ECochG. The accuracy of the I-V latency has been improved by combining ECochG with BERA to aid the detection of wave I. is independent of signal polarity and exhibits adaptation. The action potential. Clinical indications High-resolution computerized axial tomography and MRI have superseded many older otological investigative techniques and consequently removed many of the indications for EcochG. It is therefore important that the patient stays as still as possible and. It is therefore particularly useful in very young children or those with neurological disorders. This complex potential is derived from a variety of sources but in essence is an alteration of the electrical potential baseline (usually negative) in response to a sound stimulus. In current practice ECochG may be used for: 1. and comparing results between the two ears. it gives little low-frequency information (< 1 kHz) but has the advantage of being a monaural test technique and is relatively resistant to minor muscular contractions which would preclude brainstem response audiometry and is unaffected by general anaesthetic. Unfortunately. but the filter and time window settings are altered. Typically there is an increase in the summating potential with a normal action potential in the affected ear. Brainstem electrical response audiometry Brainstem electrical response audiometry (BERA) records the signals produced in the brain stem detected by electrodes placed over the mastoid. the reference electrode to the ipsilateral (test ear) mastoid process and the ground electrode to the contralateral mastoid process. ECochG is the most accurate of the electrical response audiometric techniques for threshold testing and can predict to within 5–10 dB of the psychoacoustic threshold at 3–4 kHz. This is the depolarization of the cochlear nerve and is similar in many respects to any neural depolarization. The active electrode is attached to the vertex. particularly the search for an acoustic neuroma. forehead and vertex. The summating potential. Intraoperative monitoring during surgery around the inner ear and internal meatus. Physiology The signal recorded by BERA is made up of a five-wave complex. Investigation of suspected Menière’s disease. The results are analysed by looking at the absolute values for various wave latencies. Technique The patient reclines on a bed or couch. The electrodes are surface electrodes. 3. It is also produced by cochlear hair cells and does not adapt in response to high stimulation rates. As the evoked responses are so small they are easily masked by other neuromuscular signals. The signals are usually presented using headphones to allow monaural testing.EVOKED RESPONSE AUDIOMETRY 79 2. Threshold testing. It has a threshold. 3. which is thought to represent successive synapses in the auditory pathway as follows (Jewett classification): . the so-called I-V latency.

4. but it is not frequency specific. One of the main indications for BERA is to exclude an acoustic neuroma (or other brainstem tumour) in patients with asymmetrical hearing loss. Threshold is taken as the point at which the V-potential disappears. 3. Acoustic neuroma. as such its presence can be associated with clinical hearing. Unusual results may indicate multiple sclerosis. Unfortunately.or triphasic wave commencing after 50 msec and continuing beyond 200 msec. Tone bursts are the preferred test stimuli and are presented by headphones.0 4. with active on the vertex. Fewer than 100 responses need be sampled to achieve a useful result.80 OTOLARYNGOLOGY Wave I II III IV V Site of generation Cochlear nerve Cochlear nucleus Superior olive Lateral lemniscus Inferior colliculus Latency (msec) 2.0 3. BERA can be used to define the site of a brainstem lesion depending on the presence or absence of successive waves. If feasible it offers excellent frequency specificity. Threshold testing.4 msec when compared with the normal ear.9 These potentials are very small and rarely reach more than 1 mV (potentials of 10 mV may be obtained in electrocochleography). 2. reference on either mastoid process and ground on the forehead. The technique may be used as a monitor during tumour surgery designed to preserve hearing. Cortical electrical response audiometry The cortical ERA (vertex or V potential) is a relatively late phenomenon and can be detected as a bi. it is strongly influenced by the patient’s conscious level and attendance to the stimulus and so is only of value in the cooperative patient. useful results are virtually impossible if the affected ear has very poor thresholds (> 70 dB).3 5. Brainstem lesions. staying both still and awake. In this case the I-V interval in the affected ear should be prolonged by more than 0. . Intraoperative testing. However. Clinical indications 1. as movement and consciousness level can easily influence the response. and gadolinium-enhanced MRI is a more sensitive and specific test for this condition. Technique The patient sits comfortably in a chair. perceptual cortical phenomenon. This is particularly useful in children as it is non-invasive and not influenced by anaesthetic.7 5. It is too late to be considered a primary cortical response and almost certainly represents a secondary. Surface electrodes are placed.

p. 1990. Current Opinion in Otolaryngology and Head and Neck Surgery. p. 254. 194. 2: 177–185. Menière’s disease. p. Noise-induced hearing loss. Non-organic hearing loss. Central deafness. 1.EVOKED RESPONSE AUDIOMETRY 81 Clinical indications 1. London: Butterworth-Heinemann. Related topics of interest Acoustic neuroma. . In rare patients ECochG and BERA are normal but the V-potential is absent. any more would be too timeconsuming. 239. Auditory evoked potentials. Further reading Ballantyne D. 192. In medicolegal cases this is restricted to 1. p. Hyde ML. 2. 167.2 and 3 kHz. 257. p. Radiology in ENT. p. Handbook of Audiological Techniques. 1994. p. Pure Tone Audiogram. Paediatric hearing assessment. Threshold testing.

You will be asked how you would manage the patient. Ask which is the better hearing ear. pull the pinna upwards. The pinna Examine the pinna in front and behind for signs of inflammation or skin lesions. and that you are able to present your findings accurately and clearly. The external auditory canal To examine the external auditory canal. A good view of the tympanic membrane should then be possible. the pinna has to be drawn downwards and backwards. outwards and back-wards. Common examination subjects include congenital lesions of the pinna. The mastoid process should be carefully examined for scars. position the patient to one side of an electric lamp with the light source slightly above the level of the ear. perichondritis and surgical scars. but avoid contact with the sensitive bony part of the canal. owing to non-development of the bony external meatus. who sits opposite the ear to be examined and reflects light on to it. In infants. redness or tenderness. The ear should be examined with either reflected light from a head mirror or an electric powered head light. Note any discharge from the external auditory meatus as well as any inflammation of the skin. so be thinking about this as you present your examination findings. It is not just a question of spotting the particular clinical signs or disease process. Be particularly careful not to miss a fading postauricular or endaural scar. Select a suitably sized speculum for insertion into the external canal. Introduce the otoscope speculum just past the hairs of the outer canal. The examiner will want to establish that you have an orderly and thorough technique. When using a head mirror. Time taken in practising your technique is therefore well spent. cauliflower ears. Introduce yourself to the patient before starting the examination. . The patient should be seated sideways to the surgeon. Always begin the examination with the better ear and never touch the patient before asking if there is any tenderness. Common examination subjects include canal stenosis and exostoses.EXAMINATION OF THE EAR There is absolutely no doubt that you will be asked to assess an ear at some point during the course of any ENT examination.

Examine all quadrants of the membrane. should then be performed to help differentiate between a conductive and sensorineural hearing loss. The non-test ear is masked either by using a Bàràny noise box or by pressing the tragus backwards and rotating it with the index finger. Free field voice tests. 6. a perforation or tympanosclerosis. conversation voice and shouted voice at 60 cm from the ear. Remember to tell the patient what you are doing beforehand. Introduce yourself to the patient. The long process of the incus is frequently observed behind and parallel to the handle of the malleus and it is sometimes possible to see it articulate with the head of the stapes. Perform a fistula test by applying tragal pressure or preferably use the pneumatic otoscope. In a short case examiners will sometimes stipulate that they are only interested in facial nerve function. 4. and this should always be routinely tested in examination of the ear. for example the promontory. Ascertain which is the better ear and start with this. If there is a perforation note its position.EXAMINATION OF THE EAR 83 The tympanic membrane Look for the prominent lateral process and handle of the malleus. Other tests The postnasal space should be examined to exclude a lesion and if possible to obtain a view of the Eustachian tube orifice. Tuning fork tests. Postnasal space. assess access (meatoplasty size and height of the facial ridge) and decide if the cavity is healthy or not. The cranial nerves should be formally examined if there is active ear disease. round window. Inspect the pinna. The patient sits side on to the surgeon so that lip reading is not possible. mastoid and external auditory meatus. 2. 5. If you do discover a perforation then make sure you can describe what you see looking through it. Pneumatic otoscopic examination of the tympanic membrane. Hearing tests Perform free field speech tests by asking the patient to repeat words spoken with a whispered voice. using a 512 kHz fork. Position the patient. 8. 3. incudostapedial joint. size and whether it is central or marginal. 10. Fistula test. The Rinne and Weber tuning fork tests. Facial nerve. Use double figure numbers or bisyllable words as the words the patient is asked to repeat should not be easy to guess. 9. A Siegle speculum or otoscope with a pneumatic attachment should be used to assess the mobility of the membrane. Summary of examination of the ear 1. Immobility may be due to fluid in the middle ear. dehiscent Fallopian canal or some tympanosclerosis may be visible. Look for conjugate deviation of the eyes away from the examined side and then (whilst maintaining pressure) nystagmus in the direction of the diseased side. 7. . If the patient has had mastoid surgery determine the type of cavity.

84 OTOLARYNGOLOGY Related topics of interest Clinical assessment of hearing. Examination of the nose.86. p. p. . p. Examination of the throat. 45. 84.

for example nasal polyps or a nasal tumour. the deviation of the nose. erythema or for ulceration of the skin. sneezing. Turn the patient’s head to the left and then to the right to check the profile. snoring and cosmetic deformity. headache and facial pains. hypertrophied turbinates. relevant investigations and treatments of these conditions. rhinorrhoea. abnormal sense of smell. epistaxis. a deviated septum and nasal polyps) so be thorough with your examination. be thorough in the rest of your examination. Position of the patient Introduce yourself to the patient and sit opposite with an electric lamp at eye level over the patient’s left shoulder. Be especially vigilant to look for a fading lateral rhinotomy scar or hidden bicoronal incision wound behind the hairline. A previous history of trauma or allergy may also be relevant. There may be a combination of signs (for example. Assess the mucosa. septal perforation and nasal polyps.EXAMINATION OF THE NOSE The diagnosis in nasal disease is often obvious after an accurate history has been taken. The patency of the nasal airway is assessed by occluding each nostril in turn with the tip of the thumb and asking the patient to sniff or alternatively watching the shiny surface of a Lack tongue depressor held under the nose cloud over as the patient exhales. Look for swelling. The essential symptoms are nasal obstruction. An old examination favourite is a patient with the lupus pernio rash of sarcoid on their nose. Sit with your knees together and to the right side of the patient’s legs. Common findings are septal deviation. bruising. If a lesion is immediately obvious. The nasal cavity Anterior rhinoscopy is carried out using a Thudichum speculum. note the position in relation to the turbinates and septum. Pay particular attention to its size and shape: the convexity or concavity of the dorsum. It is therefore essential that you are familiar with the aetiology. with a septal perforation. signs can be elicited quickly and management of the common diseases makes good discussion. the width or projection of the tip. Gently introduce this into the nose remembering that the nasal mucosa is very sensitive. note its . This is more elegant than sitting with your legs astride the patient’s. Nasal disease is common. Do not assume that they will be the only abnormality. the shape of the columella and nares. Lift the tip of the nose with the thumb to obtain a view of the nasal vestibules. The thickness of the skin may be relevant if cosmetic surgery is contemplated. Inspection of the external nose Examine the nose in relation to the rest of the patient’s face. postnasal drip.

Anterior rhinoscopy with a Thudichum speculum. Introduce yourself. Warm a small postnasal mirror and pass it through the mouth while gently holding the tongue down with a tongue depressor. vascularity and crusting.86 OTOLARYNGOLOGY colour. The fossae of Rosenmüller lie immediately above the tubal orifices and can be the site of a nasopharyngeal carcinoma. 5 or 10% cocaine hydrochloride or phenylephedrine with lignocaine). Postnasal space examination. In clinical practice a 0–4-mm 0° or 30° nasendoscope can be used. Examine the septum for its position in relation to the nasal airways. 6. Report the problem to the examiner and suggest that in normal circumstances you would proceed to use a flexible fibreoptic nasendoscopy after applying topical anaesthetic and decongestant to the nasal airway. 3. Summary of examination of the nose 1. In the lateral wall the tubal ridges of the pharyngeal ends of the Eustachian tubes can be seen. Oral examination Inspect and percuss the upper teeth. . Inspect the external nose. through which the posterior ends of the inferior turbinates may be visible. Oral examination. Inspect the posterior end of the septum. Drainage from the posterior part is to the middle deep cervical nodes. is it deviated to one side or is it dislocated off the maxillary crest? Examine the mucoperichondrium for its colour and vascularity. 2. 8. 7. This is a difficult procedure and needs practice. Neck. The lymphatic drainage from the anterior part of the nose is to the submandibular nodes and upper deep cervical nodes. The floor of the maxillary sinus lies over the alveolar process of the maxilla and the roots of the second premolar and first molar teeth. Assess movement of the soft palate and if there is a bifid uvula be aware that this may signify a submucous cleft.g. 5. The neck Inspect and palpate the neck and look for the presence of lymphadenopathy. Note any lesions or perforation of the septum. Some patients have too strong a gag reflex to allow adequate examination. The nasopharynx Explain to the patient what you are about to do. Examine the nasal tip and vestibule and assess the nasal airways. This will allow an inspection of the lateral nasal wall and the anatomy (and any pathology) of the middle meatus. 4. If a better view is needed the nasal mucosa can be shrunk using a local anaesthetic/vasoconstrictor (e. the posterior choanae. Examine the lateral nasal wall and evaluate the size and colour of the inferior turbinate. Position the patient.

180. Nasal polyps. 82. Nasopharyngeal tumours. p.EXAMINATION OF THE NOSE 87 Related topics of interest Examination of the ear. . p. 174. 86. p. p. Examination of the throat.

do not irritate the examiner by examining parts of the patient that have not been mentioned. vocal cord oedema. Check over the palate. Unless clearly stipulated. referred otalgia. The two tongue depressors are then used so that the buccal mucosa. dysphagia. The surgeon should sit with knees together and legs to the right side of the patient’s. Ask the patient if there is any tenderness in the mouth. teeth and alveolar ridges and the opening of the parotid ducts (opposite the upper second molar) can be examined. However. laryngeal papillomas. or an electric head light can be used. Ask the patient to say ‘aah’ and check .EXAMINATION OF THE THROAT The symptoms associated with throat disease include hoarseness. Take two metal tongue depressors and insert them to retract the buccal mucosa on each side. This should allow an inspection of the dorsal and ventral surfaces of the tongue. unfortunately applied indifferently by some examiners to the pharynx and larynx. cough. if in doubt it is better to be thorough. do not assume that the examiner merely wants an indirect laryngoscopy performed. Ask edentulous patients to remove their dentures. lump in the throat. The oral cavity Inspect the lips for perioral lesions. • Examine the patient’s neck: inspect and palpate the neck. If a head mirror is used. the tongue’s lateral borders and the floor of the mouth. Position of the patient A head mirror to reflect light from a bulls eye lamp. Remove any neck scarf which may hide a wound or stoma. occasionally patients with a neoplasm and laryngectomy patients. There are a few scenarios: • Examine the patient’s throat: systematically examine the patient’s pharynx and larynx as you would any patient in clinic who complained of the aforementioned symptoms. Expose the whole of the neck up to and including the clavicles. it also tests hypoglossal nerve function. Ask the patient to protrude the tongue and move it from side to side and then up to the palate and down. Then dispense with one of the tongue depressors and use the other to depress the tongue. vocal cord nodules. vocal cord polyps. Listen carefully to the examiner and do what is asked. Common findings are patients with vocal cord paralysis. lump in the neck and weight loss. • Examine the mouth: inspect and examine the oral cavity. The technique outlined in this topic is ideal for a long case but may need to be modified for a short case. the tonsils and the posterior pharyngeal wall. the patient should sit opposite the surgeon with an electric lamp positioned at eye level over the left shoulder. Throat is a vague term. sore throat. On the other hand.

Check that the patient does not have a stoma. Be careful not to overlook a fading wound. Inspect the base of the tongue. After a few minutes the soft palate and uvula will be anaesthetized. Be gentle. The movements of the vocal cords are studied by asking the patient to say ‘ee’ followed by a deep breath and ‘ee’ again. the aryepiglottic folds. Ask the patient if there is any tenderness. Be sure to tell the patient to avoid food and drink for the next hour because the gag reflex is impaired. Examination of the neck Check the neck for any obvious skin lesion or ulceration. If the patient nose breathes and arches up the tongue.7mm 30° rigid or flexible nasendoscope. The patient should then be requested to breathe normally through the mouth as the mirror is introduced gently up to the soft palate. A thyroid goitre may also be seen moving with the larynx. Note any inflammation. the ventricular folds and the vocal cords. Ask the patient to swallow and watch the larynx move. Examine the posterior pharyngeal wall. Ask the patient to breath gently through the nose. In these cases it may be possible after spraying the oropharynx with lignocaine. If the patient is still unable to tolerate the procedure spray the nose with local anaesthetic and decongestant and use a flexible nasendoscope. Palpate the base of tongue. above which lie the fossae of Rosenmüller. the usual site of origin of nasopharyngeal carcinoma. Warm a postnasal mirror and pass it through the mouth while gently holding the tongue down with a tongue depressor. It is unlikely in an examination that the patient will have an overactive gag reflex as patients are specially selected. Note any abnormal move-ment or fixation of the cords. ulceration or exophytic lesion. This is usually well tolerated and allows a more thorough inspection and assessment of vocal cord movement. Start at the mastoid bone and palpate down the line of the trapezius muscle and in the posterior triangle down to the clavicle. Warm a laryngeal mirror and check its temperature on the back of your hand. Some patients still need to be assessed under a general anaesthetic. Indirect laryngoscopy Explain to the patient what you are about to do. Bimanually palpate the floor of the mouth overlying the submandibular duct for calculi or masses. the arytenoids. Look for any obvious lesion. Ask the patient to count to 10 and assess the voice. Get the patient to breathe deeply in and out through the mouth and note any stridor. Feel for supraclavicular and infraclavicular nodes.EXAMINATION OF THE THROAT 89 movement of the palate. obstructing the view. and to avoid burning the throat and aspiration. Ask the patient to protrude the tongue and gently grasp it with a swab held in the left hand. the pyriform fossae. the vallecula and the upper part of the epiglottis. Postnasal space examination Explain to the patient what you are about to do. Remove the tongue depressor and put a glove on. Some patients are unable to cope with an indirect laryngoscopy because of an overactive gag reflex. it is possible to obtain some improvement by asking the patient to quietly make a’hah’ noise breathing in and out. In clinical practice the PNS can be examined by using a 2. but be particularly vigilant on inspection of the laterally placed Eustachian tube elevations. The neck should be palpated from behind and in an orderly sequence so that no areas are missed. . An enlarged neck mass may be visible: note its position and inform the examiner that you have seen it. as a tumour in this site may not be visible but easily palpable. and then both sides of the epiglottis.

Loss of normal laryngeal crepitus (Trotters sign) may indicate a postcricoid neoplasm. auscultate and listen for a bruit. 82. thyroid gland. 138. Nasopharynx. Summary of examination of the throat • • • • • • • Introduce yourself to the patient.90 OTOLARYNGOLOGY Then palpate down the line deep to the anterior border of the sternocleidomastoid muscle for deep cervical nodes. Related topics of interest Examination of the ear. Oral examination (oral cavity and oropharynx). If you think a lump is cystic see if it transilluminates. consistency and fixation to adjacent tissues or skin. preauricular nodes and finally occipital nodes. Oral cavity carcinoma. p. p. If you think a lump is pulsatile or attached to the carotid. Examination of the neck. Position the patient and expose the neck down to the clavicles. p. When your fingers reach the suprasternal notch. p. size. Laryngeal carcinoma. 197. submandibular nodes. Oropharyngeal carcinoma. laryngeal cartilages and hyoid bone. 180. . Assess speech. Indirect laryngoscopy. p. palpate up the anterior triangle. If a lump is palpated in the anterior triangle see whether it moves on swallowing. 84. feeling the trachea. 203. If a lump is felt note its site. Nasopharyngeal tumours. shape. Examination of the nose. Feel for submental lymph nodes. the parotid gland. p.

evaporation occurs to leave a sticky. Wax Wax can be secreted in one of two forms. less sticky. This is not possible in the external ear canal and so it has developed the property of epithelial migration. Impaction is commoner in males owing to the presence of thicker. usually as a result of friction from clothing or washing. It then mixes with the secretion of the ceruminous and pilosebaceous glands and any collected debris to form what we recognize as ear wax. When it reaches the hair-bearing cartilaginous portion of the canal the superficial layer starts to separate. zealous use of cotton buds and even a hearing aid mould may impede the normal flow of wax to the periphery. After secretion. The glands are found in the skin of the outer third of the external acoustic meatus and secrete a liquid material at the base of the hairs.EXTERNAL EAR CONDITIONS Ear wax This chapter confines itself to a discussion of ear wax. . Wax is then normally loosened by transmission of movement from the temporomandibular joint from chewing or talking. Foreign bodies in the ear canal. waxy substance that is able to trap dirt. keratosis obturans. squames and microbes with relative ease. Wet wax is produced by most people of African origin and caucasians and is familiar as moist. when it moves laterally. allowing its passage out of the external auditory meatus. otitis externa and conjenital abnormalities are discussed elsewhere in separate topics (see Related topics of interest). ear wax tends to become drier with age as a result of reduced glandular numbers and activity. coarser hairs in the lateral part of the external auditory meatus (EAM). The gene for wet wax is dominant. granular and brittle. Narrow canals. Squamous epithelium on the tympanic membrane moves radially until it reaches the canal walls. The dry type is more common in Mongoloid ethnic groups and tends to be greyer in colour. In some people no obvious cause is found to account for the impaction and it has been suggested that desquamation of the superficial layer of the meatal epidermis is impaired. Epithelial migration In all other parts of the body. Regardless of type. sticky and honey-coloured. the superficial keratinized squamous epithelium is constantly shed. extostoses and osteomas. This natural process can be upset by a number of factors and cause wax impaction.

The keratin takes this appearance because the part in contact with the air oxidizes and changes colour. Exostoses. on the other hand. otalgia. pain. In both conditions. In the long term these patients require periodic monitoring and aural toilet. The procedure is often best preceded by a week or two of ceruminolytic agent use (sodium bicarbonate drops are efficacious. As with collections of keratin anywhere. they rarely . These direct a jet of warm (body temperature) water along the roof or posterior canal wall so that it passes behind the wax and forces it outwards. this sets up a low-grade inflammatory response. Osteoclast-stimulating mediators are produced. This is often difficult as the patient is usually in considerable pain and a general anaesthetic is not infrequently required. a known or suspected perforation and a difficult ear. which can usually be accomplished easily by syringing. Otalgia is usually the dominant feature. Clinical features Patients usually present with an acute exacerbation of the inflammatory process. often caused by a narrow and/or tortuous external meatus. vertigo and coughing (via the auricular branch of the vagus—Arnolds nerve). are common. resulting in a resorption of bone and usually a widening of the bony canal. although the lumen of the canal may be reduced. Management Removal of the keratin plug is essential to control the inflammatory process. complications may occur and include coughing. although there is inevitably a conductive hearing loss from the occluded canal. local trauma. Contraindications to syringing include frequent previous episodes of otitis externa. otitis externa and rarely tympanic membrane perforation and otitis media. safe and inexpensive). Exostoses and osteomas Osteomas are uncommon benign tumours of bone usually arising from the tympanosquamous or tympanomastoid suture line. usually from swimming. They appear to be caused by a periosteal reaction to exposure to cold. Most of these symptoms are improved by removing the wax. They are hyperostoses of the tympanic bone of the external canal. Keratinocytes and keratin debris collect in the deep part of the external auditory meatus. In these cases removal under direct vision with an operating microscope using microsuction or waxhooks is a more appropriate and safer alternative. Topical antibiotic/steroid combinations are advised to prevent a secondary otitis externa. deafness.92 OTOLARYNGOLOGY Clinical features Impaction of wax can cause a sensation of obstruction. although wax impaction is a relatively rare cause of hearing loss. The otoscopic appearances are similar to an acute otitis externa around impacted wax. Although relatively safe. Keratosis obturans This uncommon condition occurs when there is a failure of the normal process of migration. Management Syringing involves the use of an old fashioned Higginson or a modern electric-pump syringe.

p. 1992. 209. If problems do occur they are usually related to impairment of the normal process of epithelial migration. Otolaryngology— Head and Neck Surgery. 85:346–349. p. Cerumen: its fascination and clinical importance: a review. while exostoses will more often require a formal postaural or endaural approach. Foreign bodies. Related topics of interest Examination of the ear.EXTERNAL EAR CONDITIONS 93 result in symptoms. Osteomas can often be removed via the external canal. . 82. p. 90:337–342. Diffuse exostoses and osteomata of the external auditory canal: a report of 100 operations. Journal of the Royal Society of Medicine. Mulley GP. 103. Otitis externa. 1982. In these cases surgical removal may be indicated. Sheehy JL. Further reading Hanger HC.

Communication with the vestibulocochlear nerve occurs within the internal auditory meatus. The voluntary and reflex movement of groups of muscles that normally do not contract together. If this is confirmed by an MRI scan and angiography the cause may be treated surgically. Synkinesis. it is important to appreciate that there are supranuclear or upper motor neurone (motor cortex to pontine facial nuclei) and infranuclear or lower motor neurone causes of a facial nerve palsy. It is associated with brain stem gliomas and multiple sclerosis.FACIAL NERVE PALSY Although the detailed anatomy of the facial nerve will not be discussed. Facial myokymia. These interconnections explain the mastoid. Associated features Altered facial nerve function occurs with a variety of conditions and in a variety of forms. face. It is thought to be most commonly caused by compression of the nerve by an artery in the posterior fossa. partial transection and complete transection. This is unilateral or more commonly bilateral involuntary spasmodic eye closure. but more severe injury gives no response. This is an intermittent spasm of the orbicularis occuli muscle which may spread to include other or all muscles of facial expression. For example blinking. . vagus. tympanic. The infranuclear portion can be divided into cerebellopontine angle. This may occur after neurotmesis (or more severe injury) when the axons do not find their correct endoneural sheath. mastoid and extracranial portions. Injection of botulinum A toxin into the orbicularis oculi may provide temporary relief. Extracranially there are communications with the glossopharyngeal. 3. These studies can be used to provide a prognosis and to indicate if recovery is occurring. meatal. where motor axons find the myelin sheath within the greater petrosal nerve. Hemifacial spasm. Injury may be classified into a neuropraxia. 1. Crocodile tears. axonotmesis. with the otic ganglion and sympathetic afferents from geniculate ganglion branches and with the auricular branch of the vagus nerve from a branch of the mastoid segment of the facial nerve. greater auricular and the auriculotemporal nerves and multiple communications with branches of the trigeminal nerve. ear. face and neck pain associated with herpes zoster and Bell’s palsy. 5. labyrinthine. 2. and the referred otalgia. throat and neck pain which may occur with malignant disease. 4. Cerebellopontine angle tumours may also cause this phenomenon. Lacrimation with eating can occur as a result of facial nerve injury in the region of the geniculate ganglion. neurotmesis. In this condition there are multiple fine but asynchronous facial movements. Blepharospasm. Evoked electromyography and maximal stimulation test response neurophysiological studies show that a neuropraxia injury gives normal results and an axonotmesis up to 10% of normal. may be accompanied by movement of the corner of the mouth. occipital.

normal symmetry and tone Motion Forehead: none Eye: incomplete closure Mouth: asymmetric with maximum effort Gross Only barely perceptible motion At rest. contracture or hemi facial spasm At rest. eye and mouth are used to score the dysfunction. but not severe synkinesis. Factors such as symmetry. Brackman DE.). Otolaryngology and Head and Neck Surgery 1985. Grade I—Normal II-Mild dysfunction Characteristics Normal facial function in all areas Gross Slight weakness noticeable on close inspection May have slight synkinesis. All ENT medical staff should grade all new facial palsy patients and follow-ups according to the HouseBrackmann grading system (reproduced from House JW. asymmetry Motion Forehead: none Eye: incomplete closure Mouth: slight movement No movement at all III—Moderate dysfunction IV—Moderately severe dysfunction V—Severe dysfunction VI—Total paralysis . resting tone and muscular movement at forehead. normal symmetry and tone Motion Forehead: moderate-to-good function Eye: complete closure with effort Mouth: slightly weak with maximum effort Gross Obvious. to grade 6: total paralysis. with permission from Mosby Inc. normal symmetry and tone Motion Forehead: slight-to-moderate movement Eye: complete closure with effort Mouth: slightly weak with maximum effort Gross Obvious weakness and/or disfiguring asymmetry At rest. At rest. 93:146–147.FACIAL NERVE PALSY 95 Severity grading The most commonly used system is that of House and Brackmann which grades from 1: normal function in all areas. but not disfiguring difference between the two sides Noticeable.

7. 6. Investigations A high-resolution CT or MRI scan to include the petrous temporal bone will exclude cerebellopontine angle tumours as a source of the palsy. 2. Management 1. Tumour (6%). in which a stimulating electrode is placed adjacent to the stylomastoid foramen and recording electrodes are placed either on the skin over the facial muscles or through the skin into the muscles. It is probably a virally induced immune response that leads to inflammation. usually in the parotid region. The prognosis overall for those below this level is only a 20% chance of achieving grade 1 or 2 recovery. gliomas or cerebrovascular accidents. Eye care is mandatory in order to prevent corneal ulceration and comprises artificial tears. and many surgeons will therefore advocate surgical decompression of the nerve in these circumstances. myasthenia gravis and Guillain-Barré syndrome. An acute lower motor neurone facial palsy of unknown aetiology and therefore a diagnosis of exclusion. it is important to know the severity of a palsy as soon as possible after nerve injury as this will influence the management. It recurs in 12%. These may arise from the nerve (facial nerve Schwannoma). If the EEMG response remains above 10% of normal during the first 10 days after injury there is an excellent chance of grade 1 or 2 recovery (85%). a sensorineural hearing loss. eye closure with tape on to which is applied a light pressure dressing of cotton wool. ointment at night and eye protection when outdoors on windy or hot dry days with an eye pad. Trauma (19%). It may localize injury in cases due to trauma or chronic suppurative otitis media. Facial nerve palsies caused by tumours and infection are discussed elsewhere (see Related topics of interest). altered facial sensation and taste. tinnitus and vertigo are all common in Ramsay Hunt syndrome. palate and buccal mucosa to become involved. Caused by herpes zoster virus. Bell’s palsy (55%). The communications of the facial nerve may allow the face. Central causes. A lower motor neurone facial palsy may occur with acute suppurative otitis media (in the 8% who have a dehiscent Fallopian canal). For example secondary to multiple sclerosis. chronic suppurative otitis media either with or without cholesteatoma and malignant otitis externa. For example sarcoid. external compression of the nerve (vestibular nerve schwannoma). When trauma has caused the palsy. Other causes. external ear canal oedema. is helpful. 4. drugs. but only 60% recover to House and Brackmann grade 1 or 2. sometimes necessary in suspected Bell’s palsy as this is a diagnosis of exclusion. General. This may be external or iatrogenic. or invasion of the nerve (most commonly with parotid tumours). swelling and consequent impaired function of the facial nerve. Clinical features In Bell’s palsy the facial nerve palsy is usually of rapid onset and associated with otalgia. An evoked electromyogram (EEMG). more commonly on the contralateral side. neck tongue. Infection (4%). It rarely recurs. Ramsay Hunt syndrome (synonym: herpes zoster oticus) (7%). Severe otalgia with vesicles involving the external ear associated with crusting. 3. In patients with marked symptoms a lateral tarsorrhaphy or the insertion of a gold . 5. External trauma includes head injuries or penetrating trauma.96 OTOLARYNGOLOGY Causes 1. Reassurance and explanation are essential for all patients.

4: 369–374. If a complete lower motor neurone facial palsy is noted immediately after external trauma. Although no placebo-controlled double-blind trial has been reported. Further reading Bradford CR. Current Opinion in Otolaryngology and Head and Neck Surgery. House JW. although formal decompression of the nerve is probably unnecessary. Otolaryngology and Head and Neck Surgery. (b) Ramsay Hunt syndrome. Facial nerve grading system. The facial nerve is usually sacrificed if it has been infiltrated by tumour which cannot therefore be teased off the nerve. many practitioners advocate a short course of steroids provided there are no contraindications in the patient’s medical history. A partial palsy or a delayed onset of a palsy can be managed conservatively with sequential EEMG monitoring. perhaps because significant debridement was necessary or the injury involved a significant length of nerve. a permanent facial reanimation procedure. Fisch advocates early decompression of the meatal portion of the facial nerve by a middle fossa approach. 93: 146–147. The commencement of acyclovir 800 mg five times daily for 7 days as early as possible during an attack may reduce the length of the infection and postherpetic neuralgia. (a) Bell’s palsy. Brackman DE. El-Kashlan H and Kileny P. Adequate analgesia is essential. then a cable of sural or great auricular nerve is necessary. A cable graft is indicated in these circumstances. Follow-up and aftercare If no recovery of function has occurred within a year of injury in those with a severe or complete palsy (grade 5 or 6). This must be performed without tension on the nerve. Adequate counselling regarding eye care is essential. (e) Infection. this suggests that the nerve has been severed. a palsy secondary to ASOM should be treated conservatively but that secondary to CSOM requires mastoid exploration to eradicate the underlying disease. 2. as this is the portion most often implicated as being affected in Bell’s palsy. 1994. Maximum recovery may take 12 months so that no decision regarding permanent facial reanimation procedures should be undertaken until then. . 1985.g.FACIAL NERVE PALSY 97 weight into the upper eyelid may be necessary as a permanent or temporary manoeuvre to ensure adequate eye closure. and splinting the external ear canal with a pope wick expanded with antibiotic/steroid drops will reduce the otalgia. The management in these circumstances is discussed elsewhere (see Related topics of interest). and should this not be possible after preparation of the stumps. In summary. Facial reanimation. (d) Tumour. Current Opinion in Otolaryngology and Head and Neck Surgery. (c) Trauma. Specific. 1998. e. Some groups also advocate the use of acyclovir as viral antigens have been found. may be indicated. 6:334–337. It is preferable to anastomose the proximal to the distal stump after each has been prepared to present a clean surface. Outpatient facial nerve evoked electromyography testing. temporalis muscle sling or a gold weight for the upper eyelid. and immediate exploration is indicated.

Cosmetic surgery. Chronic suppurative otitis media. p. p. . p. 5.63.98 OTOLARYNGOLOGY Related topics of interest Acute suppurative otitis media. 38.

Up to 50% of cases of facial pain never receive a definitive diagnosis. agonizing. eyes. Miscellaneous headaches unassociated with structural lesion. • Cranial neuralgias. misdiagnosed and mistreated. while the Visual Analogue Scale is the most widely-used pain intensity measure. It is unsurprising that pain arising from there is often misunderstood. sore. sinuses. Classification ication of headache Headache is a common presenting complaint.FACIAL PAIN AND HEADACHE A. . nose. He should be encouraged to use descriptive terms. neck. Headache or facial pain associated with disorder of cranium. the patient will frequently find it difficult to convey the experience of pain to the listener. and successful pain management will not be achieved without acknowledgement of this fact. If facial pain is to be successfully managed it is essential to spend sufficient time with the patient to elicit a full history. It is inevitable that the sufferer will have a significant emotional component to the pain. The International Headache Society has provided a detailed classification of headache. Cluster headache and chronic paroxysmal hemicrania. Some of the more common diagnoses and their management are discussed briefly. such as burning. cramping. When taking a pain history. nerve trunk pain and deafferentation pain. stabbing which are of more value in suggesting diagnosis than words that indicate intensity e. Tension-type headache. The McGill Pain Questionnaire attempts to define the qualitative aspects of pain. A number of pain assessment tools have been developed which may aid the clinician in accurately defining the pain. particularly if symptoms have been present for some time.g. The reader is reminded of the definition of pain issued in 1986 by the International Association for the Study of Pain which reads as follows: Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage or expressed in terms of such damage. • • • • • Migraine. ears. mouth or other cranial or facial structures (referred pain). throbbing. excruciating. teeth. tribute is paid to this fact by the plethora of treatment options.Leach The head and neck is an anatomically and neurologically complex region.

but may take the form of dysaesthesia in the ipsilateral limb or face and as a mood change) which precedes the headache by 10–60 minutes. The pain is deep and throbbing . Treatment consists of symptomatic relief with analgesics and anti-emetics. non-classifiable. It is beyond the scope of this chapter to list them all. a cranioselective 5-HT1 agonist. Only about 10% of migraine headaches exhibit the classical signs of aura (most commonly a visual phenomenon. consisting of 1–8 headaches per day for 3–12 weeks. Symptom-free periods of 3–18 months separate the clusters. Onset of symptoms is usually between puberty and the fifth decade. These changes seem to account for the symptoms of aura. Age of onset is between 20 and 40 years and there is a male-female ratio of 7:1. The headache itself is probably due to the dilatation of cranial non-cerebral vessels. there are seventeen subgroups within the ‘migraine’ section). Precipitating factors include psychological stress. associated symptoms and temporal profile. The full classification has many subgroups within each diagnostic category (for example. The characteristic feature of migraine is its throbbing nature. Diagnosis is sometimes confused with trigeminal neuralgia. A rise in cerebral blood flow in the occipitoparietal cortex precedes the headache. It lasts for 4–72 hours and the sufferer is free of pain between attacks. The aetiology is not fully understood. An impending attack may be aborted with an ergotamine preparation taken orally or by inhaler. which is effective at any stage of an attack when given by subcutaneous injection. Migraine The prevalence of migraine headache in the general population is said to be 10–15%. Prophylaxis consists largely in avoiding precipitating factors. diltiazem. It is more common in women and there is often a family history. and this is followed by a 25% reduction in flow spreading forwards from the occipital region. A careful history will reveal clear differences from TGN by duration of attacks.and phonophobia and nausea. Experimental studies in animals suggest that the trigemino-vascular system is the final common pathway where the migraine headache is generated. It takes its title from the grouping together of attacks into clusters. which is usually unilateral in onset. endocrine changes (such as menstruation) and dietary intake (especially tyramine-containing foods and irregular meals). although there is undoubtedly a vascular component.100 OTOLARYNGOLOGY • Headache associated with: • • • • • • head trauma vascular disorders nonvascular intracranial disorder substances or their withdrawal noncephalic infection metabolic disorders • Headache. Cluster headache This is a rare but important cause of unilateral facial pain. pizotifen. Drugs such as ( -blockers. methysergide and cyproheptadine have all been used in an attempt to stabilize the cranial circulation. but which may spread to involve the whole head and face and is accompanied by photo. Also available is sumatriptan.

an associated myofascial syndrome commonly develops. Trigger points are thought to arise following muscle trauma. pain on chewing or mouth opening and locking if the internal derangement is severe. Symptom relief during an attack may be achieved with oxygen. orbit or ear. Diagnosis is confirmed by observing restricted mouth-opening (less than 40mm inter-incisal). which refer either locally or to a distant site which is usually unrelated dermatomally or myotomally. For prophylaxis such drugs as prednisolone in a reducing dose. Temperomandibular joint (TMJ) dysfunction unction When anatomical disturbance of the TMJ occurs. will either reproduce the patient’s pain or refer it to a characteristic reference zone. although it may in time become bilateral as a result of a general chronic tensing of head and neck muscles and assumption of a protective posture. eliciting TMJ tenderness and clicking. Chronic tension headache does not respond well to analgesics and the most effective medication may be amitriptyline. such as poor posture or teeth grinding. TMJ problems manifest themselves as clicking or popping in the joint. pterygoids. Each attack lasts for 15 minutes to 3 hours. . forehead. it is overlooked surprisingly often as a source of chronic pain. which causes transient cerebral vasoconstriction. A sensation of fullness or congestion in the ear may be mentioned. This is described as a deep. Tension headache (also called myofascial headache) Considering that muscle accounts for about 30% of body weight. Treatment consists of physical therapy to the painful muscles and a dental splint which is usually worn at night to reposition the mandible and prevent bruxism (teeth grinding). when pressed. There are no neurological abnormalities. trapeziums and neck strap muscles. ergotamine subcutaneously or by inhaler. local anaesthetic injection or acupuncture needling of trigger points. methysergide (long-term use may cause retroperitoneal fibrosis) and calcium channel blockers have all met with some success. coupled with such techniques as deep relaxation and counselling to improve the patient’s insight into the condition. either as a single event or a repeated microtrauma. aching. In this situation psychological therapy may be required. There are always associated autonomic phenomena such as nasal congestion. If the pain has remained undiagnosed for some time it is common for a degree of pain behaviour to have developed.or bilateral. Pain is often referred forward from the occipital region to the temple. including sternomastoid. and of gradual or sudden onset. Tension headaches and migraine may be related and may co-exist. dull. or sphenopalatine ganglion block with intranasal local anaesthetic. Lack of a diagnosis rapidly results in frustration for the physician and loss of confidence in his or her abilities by the patient. Sumatriptan given by subcutaneous injection may relieve an attack. To permit this it is helpful to reduce discomfort in the muscle body with cooling spray. injected conjunctivae and facial sweating. Myofascial pain is usually associated with trigger points in the muscle and its surrounding fascia. in particular the medial and lateral pterygoid muscles. Trigger points are palpable as tender bands within the muscle which. Certain muscles appear to be particularly prone to developing trigger points. temporalis.FACIAL PAIN AND HEADACHE 101 and is extremely severe. It may appear at the same time each day during a cluster and may wake the subject from sleep. Treatment consists essentially in restoring normal function to the affected muscles by gentle stretching and mobilization. Myofascial pain usually appears on the affected side. pressure-like pain which may be uni. The assistance of physiotherapists may be useful. ice. There will usually be trigger points in associated muscle groups.

It is believed to be caused by local demyelination of the trigeminal root entry zone. The mandibular (III) division is the most commonly affected. How-ever. As with TGN. also called tic douloureux. Diagnosis must demonstrate three elements: 1. It affects men and women equally. Although rarer. Treatment should start with an anticonvulsant. Neuralgia of the nervus intermedius is felt deeply in the ear. Carbamazepine (100–400 mg tds) is the most widely used drug. although patients must be warned that symptom relief will be accompanied by sensory loss to the affected part of the face. Pain is elicited by normally-innocuous stimulation of a trigger zone. causing an antidromic infection along the nerve. lasting for seconds or minutes.102 OTOLARYNGOLOGY Trigeminal neuralgia (TGN) The principal sensory nerve to the head is the trigeminal nerve. MRI of sufficiently high resolution may demonstrate such a vessel. Gabapentin (100– 300 mg tds) has had promising results in treating neuropathic pain and has been awarded a product licence for this indication. Glossopharyngeal neuralgia (GPN) is characterized by stabs of pain in the ear. It presents with itching. TGN. pain. base of skull tumours and vascular anomalies such as aneurysms and vertebrobasilar atherosclerosis. In the first half of the last (20th) century. Acute herpes zoster Most individuals acquire varicella zoster virus during childhood infection with chicken pox. with a trigger zone in the posterior wall of the auditory canal. dysaesthesia and paraesthesia along the course of the affected nerve. The pain can induce spasms of the facial muscles on the affected side (hence tic). although it has been described outside these age limits. Infection is commoner in the elderly and the immunocompromised. acoustic neuroma. tortuous artery or vein in the posterior cranial fossa. as malnutrition due to inability to swallow is a distinct possibility. followed by the maxillary (II) and ophthalmic (I) divisions. and less invasive treatments are the rule. surgery of this nature carries significant morbidity. swallowing and coughing. 2. If a vascular loop has been demonstrated by MRI. although other anticonvulsants such as clonazepam and phenytoin have been used. Alternatively. Pain occurs within one or more divisions of the trigeminal nerve. is an agonizingly painful condition which usually affects 50–70-year-olds. followed a few days later by cutaneous vesicular eruptions. other cranial nerves may give rise to neuralgia whose manifestation is identical to TGN. 3. decompression of the nerve root via posterior fossa craniotomy has a high chance of prolonged symptom relief. tonsillar fossa or beneath the angle of the mandible. especially in the elderly. Pain is described as a brief intense electric shock or knife-like sensation. It appears that the virus may lie dormant in the dorsal root ganglia of peripheral nerves for many years until opportunistically reactivating. base of tongue. It has been suggested that GPN may be associated with an unusually long styloid process irritating the nerve. an aberrant vascular loop may be demonstrated near the nerve’s origin. Side-effects may be problematic. it was associated with a high incidence of suicide. especially in the elderly patient. necessitating a repeat. or radio-frequencey diathermy are usually effective. Bilateral symptoms are rare. before effective remedies were widely available. destructive lesions to the Gasserian ganglion with alcohol or glycerol injection. Adequate pain relief is important. Pain commonly returns 6 months to 5 years after this. most usually due to compression by a small. Triggers include talking. and may also help to exclude other causes of these symptoms such as multiple sclerosis. These form scabs .

Constitutional upset frequently accompanies acute zoster and it may take weeks or even months for an elderly patient to recover fully. Anticonvulsants such as carbamazepine. Related topics of interest Functional endoscopic sinus surgery. Postherpetic neuralgia (PHN) Diagnosis of PHN is rarely difficult. gabapentin and valproate may help lancinating pain. It is more likely to develop in elderly patients. and two studies indicate that women are affected more than men in a ratio of 3:2. Analgesics and acyclovir should be given systemically. and examination must always include full assessment of cranial nerve function.e. and as an attempt to diminish the development of post-herpetic neuralgia (vide infra). It is thought that this phenomenon is caused by alteration of the modulating effect of large-diameter sensory nerves (proprioception) at the dorsal root entry zone (i. . both as an analgesic for the acute condition. which may account for the increased incidence of PHN with advancing years. A recent history of herpes zoster infection is followed by the development of pain in the affected area. although such relief is limited to its duration of action. although attempts to confirm this finding have been inconclusive. Treatment of acute zoster consists of pain relief and in speeding resolution of skin lesions. Care-ful consideration must be given to the history and symptomatology. extracted from chilli peppers. uncontrolled studies have suggested that aggressive early therapy reduces the incidence of postherpetic neuralgia. Sinusitis. The incidence is reported as being up to 50% following acute infection.FACIAL PAIN AND HEADACHE 103 within a week or so and heal within a month. although they undoubtedly influence neurotransmitter systems high in the CNS. the pain gate is held wide open) following viral damage during the acute infection. Early treatment with tricyclic antidepressants has been recommended. Treatment of burning pain and dysaesthesia is best achieved with tricyclic antidepressants such as amitriptyline in the lowest effective dose. It is most effective in treating burning pain. which acts by depleting substance P levels (an important neurotransmitter in pain fibres). the ophthalmic division of the trigeminal nerve and the fourth to tenth thoracic nerves are more commonly affected than others. p. but treatment often defies the efforts of the most determined physician. There is commonly an accompanying sensory deficit and allodynia (pain caused by a normally innocuous stimulus) to light touch is often a feature. p. and techniques such as transcutaneous electrical nerve stimulation (TENS) and acupuncture may also be of value. For reasons which are not understood. Pain in ophthalmic zoster is relieved by stellate ganglion block with local anaesthetic. The ability of nerve fibres to repair themselves diminishes with age. though this may take longer in the immunocompromised patient. A number of small. The pain experienced is usually burning. since the incidence of dose-related side-effects is high in the elderly. Also available is a topical preparation of capsaicin. The mechanism of action of these drugs is unknown. but occasionally throbbing or stabbing. 285. Summary This is by no means a complete guide to diagnosis and treatment of facial pain. 108.

beads. or soft organic objects such as sponge. This is initially mucoid. wood. metal. If nothing is visible then an auriscope may give a better view. Examination of the anterior nares is often possible with a head mirror or electric head lamp. They may be inorganic or organic. It is possible in many children to remove the foreign body without the need for general anaesthesia. They are often asymptomatic and may be discovered only accidentally during an examination for an unrelated complaint. It is passed point downwards above the foreign body. plastic from toys. which will require removal under general anaesthetic. The child sits on either a parent’s or nurse’s knee. and nuts. Inflammation and infection of the paranasal sinuses may complicate the problem. Organic foreign bodies include sponge. Treatment Removal is best accomplished with a wax hook or an old Eustachian tube catheter. reflecting light on to the elevated tip of the nose. Inorganic foreign bodies include buttons. . rubber. paper.FOREIGN BODIES Foreign bodies in the nose Nasal foreign bodies are most commonly found in 2. and stones. A unilateral nasal discharge is nearly always due to a foreign body. In every case the nasal cavity must be examined afterwards as there may be a second foreign body more posteriorly. Management Confirmation of the presence of the foreign body is from the history and examination of the child. which is brought to the floor of the nose and raked anteriorly. These are irritant and the nasal mucosa usually becomes involved in an inflammatory reaction causing a nasal discharge. The child should be discharged with a supply of Naseptin nasal barrier cream and oral antibiotics if there is any obvious infection. such as buttons. The first effort will be the best and often the only attempt the child will allow. Cupped forceps are preferable for the removal of thin objects. Have good illumination and all the instruments possibly required to hand. but will eventually become mucopurulent and finally odiferous mucopus.to 3-year-old children. which may be blood stained. Occasionally deposits of calcium and magnesium carbonates and phosphates takes place around a foreign body to form a rhinolith. The child must be cooperative and the surgeon gently reassuring. peas. If this fails or if the foreign body is situated posteriorly in the nasal cavity then a general anaesthetic will be required.

usually an adult. with the object viewed with an operating microscope. rubber. but a general anaesthetic may be required for children and sensitive adults. Once the object is out. a tongue depressor and laryngeal mirror should reveal the offending bone. will be able to localize the side and site with reasonable accuracy. Inorganic foreign bodies are often asymptomatic. If the patient can-not tolerate indirect laryngoscopy and a foreign body is suspected in the vallecula or base of tongue. but usually requires the skills and facilities of a specialist. Removal may appear to be easy. crayons and stones). most foreign bodies can be removed by syringing. but organic objects may give rise to otitis externa by local irritation of the epithelium of the meatal walls. If this too is normal they should be . The objects found can be organic (pieces of paper. Management The patient. 111-directed attempts at their removal by the untrained may lead to complications. peas and beans) or inorganic (beads. vallecula or pyriform fossae. seeds. If there is an otitis externa a swab should be taken. Foreign bodies in the pharynx Sharp and irregular foreign bodies may become impacted in the tonsils.FOREIGN BODIES 105 Foreign bodies in the ear Foreign bodies are inserted into the ears more commonly by school children than by toddlers. and antibiotic-steroid ear drops should be instilled. Management A foreign body in the external ear canal is usually easily seen on otoscopy. It is sometimes possible to remove the foreign body in the clinic. cotton wool or sponge. Large objects lying superficial to the external ear canal isthmus should not be syringed as there is a danger of wedging them in that area. It is rarely necessary to extract a foreign body through the posterior canal wall after a postaural incision. This is useful if permeatal extraction is not possible because of swelling of the canal walls from irritation. Objects of vegetable origin. One of the commonest causes of this is cotton wool. Forceps should never be used to remove smooth spherical objects such as beads. buttons. Treatment As a general rule. beans and nuts. Forceps are useful for soft material such as paper. Small fish bones are the commonest and usually lodge in the tonsil. so must be killed or anaesthetized with chloroform water prior to syringing. A thorough examination with light reflected from a head mirror. Insects should be killed before syringing by instilling spirit drops into the ear canal. and it is not unusual to find this in adult patients who have been attempting to clean their ears. the tympanic membrane should be examined to ensure it has not been damaged. or if a large object has lodged at the isthmus. to remove material of vegetable origin and large objects which lie superficial to the isthmus. In some patients there will be no abnormal findings and a lateral soft-tissue radiograph is indicated. Maggots grip on the external ear-canal skin. pencil. base of tongue. are hygroscopic and should not be syringed. as they will tend to push them further down the ear canal. Suction or a fine hook may be used. then examination with a nasendoscope is useful. the ear should be cleaned. such as peas.

Treatment After the foreign body has been visualized. for example a stricture. Dysphagia may be total. If the foreign body has caused a tear. It is then often possible to grasp the foreign body with forceps and remove it swiftly and painlessly. The presence of an abnormality in the patient’s aerodigestive tract. but may also occur at the level where the oesophagus is crossed by the left main bronchus or at the cardia. but pooling in the pyriform fossae on indirect laryngoscopy is sometimes evident. The foreign body may cause coughing and excessive salivation. Clinical examination may be normal.106 OTOLARYNGOLOGY reassured and reviewed 2 days later. Barium swallow as an investigation is condemned because it makes . but if there are persistent symptoms the patient should be re-examined. This has its own light source and may help locate a foreign body in the pharynx. surgical emphysema will be shown radiologically. By this time the sensation will usually have passed. Some foreign bodies are easily identified because they are radio-opaque. the pharynx should be anaesthetized with lignocaine spray. The inexperienced may confuse calcification in the laryngeal cartilages with an opaque foreign body. There may be localized tenderness in the neck and crepitus owing to surgical emphysema if there has been an oesophageal perforation. Children and psychiatric patients may not be so reliable. Investigations Lateral and anteroposterior soft-tissue radiographs of the neck and chest radio-graphs are mandatory. Mentally handicapped and some psychiatric patients are at particular risk. Patients who have been anaesthetized with lignocaine spray should be warned not to eat or drink for 2 hours as the pharynx will be relatively insensitive. Widening of the postcricoid space or a persistent air bubble in the oesophagus may occur. Impaction is commonest at the level of the cricopharyngeus muscle. The commonest objects are coins in children and fish or meat bones in adults. A large bolus of food swallowed hurriedly may become impacted even in a normal oesophagus. Discomfort or pain in the oesophagus and difficulty in swallowing are the cardinal symptoms. Foreign bodies in the oesophagus Impaction of a foreign body depends chiefly on the size and shape of the object. The surgeon’s free hand can then be used to remove the object with forceps. will make impaction more likely. Some fibreoptic nasendoscopes have a side arm which facilitate forceps and can be used to remove foreign bodies. General anaesthesia is required to remove a foreign body from the pharynx if the patient is young or unable to tolerate the above manoeuvres. Clinical features Adults are usually aware of having swallowed something and can localize fairly accurately the level at which it is impacted. In a patient anaesthetized with lignocaine spray and positioned on a flat bed with the neck and shoulders supported on a pillow it is sometimes possible to pass the blade of a McGill laryngoscope to depress the tongue.

the foreign body may pass symptomless into the trachea. if there is a good history suggestive of inhalation of an object. Opaque objects are easily identified. or a wheeze. The neck should be examined to exclude surgical emphysema on the day of discharge. If there is sharp or bony object. Adults usually give a clear history of foreign body inhalation. Vegetable foreign bodies are particularly dangerous (nuts. followed by consolidation. A foreign body may partly occlude the bronchus and act like a valve so that the partly obstructed lung becomes overinflated. There may. If there is a mucosal injury the patient should have antibiotic cover. Clinical features After the initial inhalation. which causes choking and coughing. Foreign bodies in the trachea and bronchi Inhalation of a foreign object is most common in children under the age of 3 years. . the patient requires an oesophagoscopy as soon as possible. The event can easily escape a parent’s notice. Some surgeons have suggested that the ingestion of cola fizzy drinks will encourage this process. be a cough with inspiratory and expiratory stridor. vegetables. Radiolucent objects are suspected when there is unexplained atelectasis. Most inhaled foreign bodies enter the right main bronchus. fruits) as they will cause an intense inflammatory reaction of the bronchial mucosa leading to a pneumonitis. Perforation of the oesophagus should be treated with intravenous antibiotics and nasogastric feeding. pips. Surgical repair should be considered depending on its site and extent. however. The scope and the foreign body should be withdrawn in unison under direct vision. Any unexplained choking fit on the part of the child should be treated with suspicion. mediastinal shift or consolidation of the lung. The patient should have a barium swallow 2 weeks later to exclude an oesophageal neoplasm. The patient should remain in hospital for 24 hours postoperatively and receive nil by mouth for the first 4 hours and only water for the next 4 hours. obstructive emphysema. A foreign body which is causing a complete obstruction of a bronchus will produce a collapse of that lung segment. the safest treatment is to admit the patient and give a dose of intravenous hyoscine butylbromide and diazepam. For this reason.FOREIGN BODIES 107 subsequent oesophagoscopy and identification of a foreign body more difficult. and sometimes cyanosis. which is larger and more vertical than the left. especially if any small object with which the child happened to be playing cannot be found. though Omnopaque 500 contrast medium can be used because it is clear. Treatment If the obstruction is due to an impacted food bolus. This will usually allow the oesophagus to relax and permit the passage of the bolus. Investigations Lateral and anteroposterior chest radiographs are mandatory. Using a rigid oesophagoscope the foreign body is identified and if possible drawn into the end of the scope using forceps. the child should have a bronchoscopy.

A tracheostomy may be needed if there is oedema or obstruction of the larynx. Endoscopy and removal of foreign bodies. Garret CG. Current Opinion in Otolaryngology and Head and Neck Surgery. Storz or similar instruments with Hopkins rod telescopes should be available with young children. A senior ENT surgeon and anaesthetist are required. 1998. either prior to or after bronchoscopy. p. suction tubes and forceps appropriate to the nature of the foreign body and size of the patient need to be readily available. A variety of bronchoscopes. p. Antibiotics and physiotherapy may be necessary if there is any sign of pneumonitis. Related topics of interest Paediatric airway problems.108 OTOLARYNGOLOGY Treatment Bronchoscopy should be performed as soon as possible. 6:416–420. Flexible fibreoptic bronchoscopes are used in some centres. Paediatric endoscopy. 237. Removal via a thoracotomy is sometimes necessary if the foreign body cannot be retrieved by endoscopic methods. 232. Further reading Spector BC. .

which allow drainage and ventilation. frontal sinus and sphenoid sinus infection. between the ethmoid bulla and the middle turbinate. which does not reline with ciliated respiratory epithelium. Mucosal stripping leaves exposed sinus bone. which aims to provide ventilation and drainage of the ethmoid sinuses and the secondarily involved maxillary. Common locations for contact areas in the sinuses include the frontal recess and ethmoidal infundibulum. the cleft between the uncinate process and the middle turbinate. Disease of these pre-chambers may interfere with ventilation and drainage of the dependant sinuses and cause acute or chronic mucosal disease. but usually a low columnella non-ciliated epithelium. Anatomical variance of the middle turbinate. . normal anatomy and to preserve mucosa. The frontal and maxillary sinuses communicate with the nose through a complex system of narrow clefts. Scarring and non-ciliation may lead to an irreversible impediment of ventilation and drainage. The emphasis of surgery is to preserve. The incidence of these variants is the same between a population with no history of sinus disease and a population with recurrent acute or chronic sinusitis. as far as possible. If extensive contact of opposing mucosal surfaces occurs. Pathophysiology Mucus produced in the maxillary sinus is transported from the floor of the sinus along the sinus walls. are not thought to predispose to sinusitis. the ciliary beat activity may be impeded so that spaces are blocked and do not drain. disease spreads from the nose to the paranasal sinuses. and in the lateral sinus.e. Persistent mucosal disease of the ethmoidal infundibulum. These clefts are only a few millimetres wide and contain opposing mucosal surfaces lined with ciliated respiratory epithelium. The anterior ethmoid sinus air cells and clefts are regarded as pre-chambers of the dependant frontal and maxillary sinuses. emphasising the importance of good surgical technique. whatever the cause. uncinate process and the ethmoid bulla are common. to the natural ostium by the mucous ciliary transport. i. while of academic interest. Endoscopic sinus surgery is minimally invasive surgery. frontal recess and posterior ethmoids may predispose patients to recurrent maxillary. Therefore anatomical variations. which lies above and behind the ethmoid bulla.FUNCTIONAL ENDOSCOPIC SINUS SURGERY Principle Most infections of the sinuses are rhinogenic. disease of the posterior ethmoid sinuses may interfere with ventilation and drainage of the sphenoid sinus. frontal and sphenoid sinuses. Similarly.

In patients who have failed maximum medical therapy for recurrent acute or chronic rhinosinusitis or polypoidal rhinosinopathy. Variations from the standard protocol might be necessary from time to time. for example frontal recess surgery and posterior . Revision cases can be challenging. Sinus mycosis. particularly if primary surgery performed by inexperienced surgeons has caused a lack of anatomical land-marks. significant scarring and narrowing of natural ostia due to mucosal stripping. Endoscopic optic nerve decompression. for example 1 or 2 mm coronal cuts of the frontal recess might be requested in difficult revision cases. but more extensive surgery. Endoscopic dacryocystorhinostomy. Mucoceles. These include those with malignant sino-nasal tumours and those with inaccessible lateral frontal sinus disease. Polypoidal rhinosinopathy. with two axial cuts to allow the orientation of the internal carotid artery and optic nerve in the region of the posterior ethmoid and sphenoid sinus to be identified. most commonly for dysthyroid eye disease. A common protocol would be a coronal CT scan with 5 mm cuts of 1 mm thickness. Endoscopic drainage of an orbital abscess. Chronic rhinosinusitis. Endoscopic orbital decompression. Extensive experience and expertise is necessary in basic endoscopic sinus surgery before training in extended applications is undertaken. Patients should have agreed to surgery if the CT scan confirms this is necessary. Endoscopic arrest of CSF rhinorrhoea. Endoscopic bipolar diathermy for posterior epistaxis. a CT scan should be requested to confirm that there is persistent disease amenable to endoscopic sinus surgery (the scan will provide details of sinus anatomy and disease extent).110 OTOLARYNGOLOGY Indications for endoscopic sinus surgery • • • • • • • • Recurrent acute rhinosinusitis. for example lateral frontal sinus mucoceles. Certain patients may not benefit from endoscopic surgery. Surgical technique Surgery limited to the anterior ethmoids may be performed under local anaesthetic with topical vasoconstriction and sedation. Adjuvant surgery to allergy treatment. Investigations A high definition CT scan of the paranasal sinuses on bone setting is required before undertaking endoscopic sinus surgery (except for the treatment of epistaxis). Endoscopic pituitary surgery. Antrochoanal polyps. Extended applications • • • • • • • Endoscopic spheno-palatine artery ligation for epistaxis.

• Epistaxis. Many complications occur due to not recognising sinus anatomy. Although it is an extremely efficient way of clearing soft tissue disease. In experienced hands the micro-debrider can be used for a complete sphenoethmoidectomy. • Penetration of the lamina papyracea to cause periorbital bruising or an orbital injury such as a medial rectus or an optic nerve injury. Major complications are particularly likely to happen once the surgeon has gained some confidence and experience in the technique. Through-cutting instruments which cleanly cut through mucosa and bone of sinus air cells. • Bleeding. The majority of experienced endoscopic surgeons in the UK have both through cutting instruments and the microdebrider to hand during surgery. but has not yet learned the finer points of anatomy. and in particular polypoidal rhinosinopathy. Surgery is performed in a stepwise manner from front to back (Messerklinger technique) or from the sphenoid forward (Wigand technique). namely the internal carotid artery and optic nerve. or when to stop during a procedure. Blindness and diplopia from per-operative complications will only become apparent on patient waking. and prevent avulsion and stripping of mucosa are a recent advance. Per-operative • Anaesthetic reaction. If the surgeon is uncertain as to the anatomy. its detractors claim its usefulness for bone work is not proven as it may cause excessive scarring. • Nasolacrimal duct injury. then he should ask for advice. It is much better to complete the surgery with a second stage procedure than to cause a major complication at the initial procedure. The aim of surgery is to re-establish ventilation and drainage of the affected paranasal sinus group. Complications may be reduced by a thorough understanding of sinus anatomy. The inexperienced surgeon should be closely supervised by an experienced endoscopic sinus surgeon. extensive cadaver dissection and observation of experienced surgeons in the surgical technique. in the unwary.FUNCTIONAL ENDOSCOPIC SINUS 111 ethmoid surgery requires a general anaesthetic. It may. . 2. Attendance at a post graduate course would be of considerable benefit to those who are novices in endoscopic surgery. or if this is not available then stop the operation. Immediate post-operative • Intraorbital bleeding. • CSF leak due to penetration of the skull base. 1. or to working in a poor surgical field. • Injury to structures impinging upon the lateral sphenoid sinus wall. The microdebrider cleanly cuts and aspirates tissue suctioned into the debrider opening. due to intra-operative bleeding. Complications Complications of endoscopic sinus surgery may be life threatening or cause significant long term morbidity to patients. cause disastrous orbital injuries by rapidly sucking and debriding the orbital contents if the lamina papyracea is breached. or cannot visualise landmarks due to bleeding.

• Recurrent disease. Some authorities still propose de-crusting of the ethmoid cavity every few days following surgery. • Intracranial infection (meningitis. Early post-operative • CSF leak (sometimes an unrecognised intra-operative complication). A CSF leak is the commonest major complication of endoscopic sinus surgery. It is most likely to happen when the artery is divided when lying within a bony canal running from the orbit to the anterior cranial fossa. perhaps with division of the orbital septum in the lower lid. CSF rhinorrhoea. The lamina papyracea is removed and a formal orbital decompression performed with incision of the orbital septum as for dysthyroid eye disease. or to use temporalis fascia and muscle. to allow the orbital contents to flow laterally and anteriorly. Since the surgeon has already performed an ethmoidectomy and the lamina papyracea is exposed. This will allow orbital fat and soft tissues to herniate into the ethmoids and will also provide drainage for any continued bleeding. between the middle turbinate and septum. Most surgeons now feel that this delays mucosal healing and removal of adherent crusts may predispose to greater scarring by . However. A lumber drain is usually unnecessary. If the leak is identified at the time of surgery then the site of the leak should be confirmed and the leak arrested. • Sequelae of per-operative and early post-operative complications. An intra-orbital bleed caused by such an event will cause the eye to rapidly bulge and become tense. particularly within the ethmoidal cavity. it can be removed endoscopically. Tisseel glue may be used to obtain a good seal with a piece of silastic used to separate the graft from intranasal packing. but the commonest methods are using a middle turbinate flap. It has been recommended that a lateral canthotomy be performed. Intraorbital bleed. This is one of the most feared complications of endoscopic sinus surgery and occurs when the anterior ethmoid artery has been divided during surgery and retracts into the orbit while continuing to bleed. most surgeons will not have seen nor performed this procedure before and with a patients vision in immediate danger it is arguably not the time to start. and rapid decompression of the orbit is ne-cessary to save the patient’s vision. brain abscess).112 OTOLARYNGOLOGY 3. Follow up and after care Epithelialization of the ethmoid cavity is usually complete within 3 or 4 weeks of surgery. Endoscopic orbital decompression has the dis-advantage of making identification of the bleeding anterior ethmoid vessel more difficult should a subsequent search be made for the vessel via an external approach. 4. Most would advocate an external ethmoid approach to the anterior ethmoid artery which is diathermied or ligated. as in these circumstances there will be no soft tissue attachments preventing the artery from retracting into the orbit. There are many techniques described to arrest the CSF leak. which is left in situ for several days. 2. An endoscopic medial approach is an alternative for the experienced. Management of major complications 1. or a free turbinate graft to plug the defect. Late complications • Intranasal adhesions. or between the lateral nasal wall and nasal septum.

It can locate the frontal sinus ostium. This perception may change if a system is developed which can be set up rapidly in theatre or if medico-legal developments make it a requirement. Related topics of interest Allergic rhinitis. Further reading Zweig JL. Barnes EL. Pasquale—Niebles K. p. to remove nasal crusts and secretions is advised. p. Microdebrider technique: implications for endoscopic sinus surgery. 1:27–33. Post operative steroids and antibiotics may be indicated depending on the surgeon’s preference and the underlying disease process. Sinusitis. Nasal polyps.. Sillers MJ. This system will be of especial use in patients with difficult anatomy and in revision cases. Future developments The past three years has seen major advancements in the development of image guidance systems which provide three-dimensional images of the location of a probe within the sinuses. Rhinol 2000. Post operative nasal douching. J. Schaitkin BM. morning and night. Bhuta T. J. 11. Its application is currently not justified for routine endoscopic work.Neuman AM. 174. Imageguided transnasal endoscopic surgery of the paranasal sinuses and anterior skull base. the sphenoid sinus and the skull base. Yang F. This usually allows the ethmoid cavity to heal and to become crust-free at 2 weeks post surgery obviating the need to remove persisting crusts. Rhinol 1999. . Am.FUNCTIONAL ENDOSCOPIC SINUS 113 causing delayed healing. 285. p. Am. 6:449–455.

although it may be felt higher and to be unilateral. Disorders of motor function have certainly been demonstrated in globus patients. usually in their fifth decade. true difficulties are never a feature. including elevation of cricopharyngeal sphincter pressure. Occasionally tenosynovitis of the digastric tendon as it runs through its sling on the hyoid may be the cause. In particular. This can be very rewarding to treat with a local anaesthetic/steroid injection. although one must be alert for any physical cause for the symptom such as a foreign body or an inflammatory cause. the two most strongly supported are the suggestion that it represents a manifestation of reflux oesophagitis or is a disorder of pharyngeal and oesophageal motility. The sensation is often intermittent and variable in severity. mid-oesophageal dysmotility and poor lower oesophageal sphincter relaxation. In this group of patients a vicious cycle is created where somatic concern and anxiety only serve to further aggravate the symptom. Pharyngeal pH measurements tend to be normal in such patients.GLOBUS PHARYNGEUS Globus pharyngeus (globus syndrome. a neoplastic lesion should be excluded. This cycle of events is very similar to that seen in tinnitus and thus may represent another disorder of perception. neuroticism and even depression. for many the symptom actually improves during feeding. What is undisputed is that globus patients have much higher levels of psychological distress (than the general population) in the form of anxiety. Pathophysiology A number of organic aetiological theories have been proposed. . Although patients may complain of some subjective difficulty in swallowing. It is the patient’s psychological profile that dictates whether it becomes a problem. somatic concern. usually at the region of the sternal notch. which is what many of these patients are most concerned about. discomfort or foreign body in the throat for which there is no obvious cause. globus hystericus) is the sensation of a lump. The complaint is typically of a lump in the throat. but there is still debate as to whether these are primary or secondary phenomena. Many people suffer from globus sensation for whatever underlying reason at some time in their life. Clinical features Patients are more often women. Physical examination is normal. Many patients seem anxious and introspective.

Related topics of interest Hypopharyngeal carcinoma. 17:105–106. 1992. Pharyngeal pouch. Antidepressants may be required for those patients who are clinically depressed. lansoprazole or omeprazole). ranitidine) or a proton pump inhibitor (e. Strong and appropriate reassurance at all stages is invaluable. p. H2 antagonists (e. Globus sensation.g.GLOBUS PHARYNGEUS 115 Investigations Most clinicians would perform a chest radiograph and a barium swallow in spite of a typical history and a normal clinical examination and the likelihood that these will be normal. Further reading Wilson JA. 246. endoscopy is indicated. and followup is not usually required. 124. Smoking should be discouraged. Follow-up and aftercare Most patients are happy once reassured that they do not have cancer or other serious pathology. In those patients with persistent or suspicious symptoms. Clinical Otolaryngology. Reflux oesophagitis should be treated with antacids. . The radiologist should be encouraged to pay particular attention to the hypopharynx during the examination. Relaxation therapy can be suggested for those who are tense and over-anxious. Management There is no specific treatment for globus pharyngeus. Ambulatory pH measurement and manometry are sometimes used although they rarely add much to the clinical picture.g. p.

HALITOSIS

Aetiology and pathophysiology Halitosis is a problem that not uncommonly presents to the ENT surgeon and may be subjective or objective. The causes can be divided into three broad categories: local, general and drugs. Local and general causes overlap when general or systemic conditions give rise to a dry mouth. 1. Local causes. Saliva plays a crucial role in the oral cavity and is involved in taste, lubrication, water balance and oral hygiene. Saliva acts as a mechanical cleansing agent, its contained buffers combat acid/ alkali excesses and the secreted immunoglobulins have an important anti-infective function. Any significant reduction in salivary flow allows an increase in the local bacterial flora. These micro-organisms break down proteins with the production of odiferous volatile gases and consequent halitosis (as well as leading to an increase in dental caries and periodontal disease, in themselves a cause of halitosis). A decrease in saliva production can occur temporarily, as during sleep and with anxiety, or more permanently as a result of previous radiotherapy, cardiac and renal failure and some autoimmune conditions (Sjögren’s syndrome). Any local inflammatory lesion is likely to become secondarily infected and lead to halitosis. Examples include any oral ulcerative lesion (from aphthous to neoplastic), tonsillitis, pharyngitis and nasal and sinus infections. 2. General causes. Certain foods, alcohol and cigarettes all give rise to a characteristic unpleasant smell on the breath. A reduction in food intake during any systemic illness will lead to ketosis and typical ketotic breath. Diabetes can lead to a sweet acetone smell, uraemia a smell of ammonia, liver failure a smell of decaying blood and chest infections a peculiarly foul anaerobic smell. The latter is particularly common in bronchiectasis. Reflux of partially digested stomach contents into the oesophagus as a result of hiatus hernia is another cause. There are some patients who complain bitterly of halitosis for which there is no objective support. This may represent a monosymptomatic hypochondriacal condition, and these patients may be severely depressed. 3. Drugs. Drugs can cause halitosis by several mechanisms: they may cause a dry mouth (anticholinergics), they may alter the normal oral and pharyngeal flora (antibiotics) or their metabolites may be excreted by the lungs (chloral hydrate, iodine-based medications). Clinical features Halitosis is usually due to local causes. It is commonest in those with poor dental hygiene and peridontal disease. There is a natural decline in salivary flow and increase in dental disease with age. A full history should be taken to establish any possible systemic or drug causes. Clinical examination should establish

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objective evidence of halitosis. A useful manoeuvre is to ask the patient to breathe through the mouth and the nose separately; if the smell is still present when breathing through the nose, an extraoral cause should be suspected. Investigations Investigations should be directed at the suspected cause and might include a chest radiograph and blood tests to exclude systemic disease. Management Management should obviously be directed at the underlying cause and will often fall outside the remit of the ENT surgeon. Those with systemic causes and severe chest disease will require referral to an appropriate physician. Patients with a psychological problem may require referral to a psychiatrist. Periodontal disease will require the services of a dental practitioner. Most oral inflammatory conditions will resolve spontaneously, but any that persist demand biopsy and subsequent definitive treatment. Pharyngitis, tonsillitis and sinonasal disease can all be treated appropriately by the ENT surgeon. General advice on adequate dental care, good fluid intake should be given. In some patients with objective halitosis and little pathology, a lengthy (2 to 3 months) trial of low dose antibiotics to alter the local bacterial flora can be helpful. Follow-up and aftercare This will be dictated by the underlying cause. Further reading
Symposium on dry mouth and halitosis. The Practitioner, 1990; 234:603–619.

Related topics of interest Sinusitis, p. 285; Intrinsic rhinitis, p. 131; Tonsil diseases, p. 330.

HEARING AIDS

A hearing aid is any device that amplifies sound or assists the hearing-impaired individual, but in the present context will be taken to mean an electro-acoustic device used to amplify sounds. Cochlear implants can be included in this definition, but they are described in a separate topic. Design It is important to be familiar with the basic design of the hearing aid as many patients attending the ENT department are prescribed them. There is a good chance you will be handed one and asked to describe it in an examination. The basic components of any hearing aid are a receiver (microphone and/or induction coil), an amplifier/ processor, a sound transmitter (earphone, bone conductor) and a power source (primary cell). There are two types of signal processing systems—analogue and more recently digital. 1. Analogue systems. In analogue systems, an acoustic signal is converted to its electrical analogue at the microphone stage of the hearing aid circuit. That is, an acoustic signal is constantly varying in sound pressure. When converted to an electrical analogue, the varying sound pressure is changed to a varying voltage. The amplitude of these voltages can be controlled so as to emphasize selected frequency regions, as well as carrying out other processing tasks. In order to avoid the problem of excessive amplification of loud sounds which may cause discomfort to the user, analogue amplifiers can use one of two methods of reducing sudden peaks of sound. (a) Peak dipping. In essence this system basically chops the tops off the peaks of sound. It has the advantage of being simple and instant but does result in some distortion. (b) Automatic gain control This system involves some complicated circuitry that picks up the signal and compresses it so that the maximum sound peak is never above a set maximum value. It is a little more complicated but produces less distortion. The external controls are usually a selector switch and a volume control. The selector switch has three markings; O is for off, T is for a television or telephone induction coil and M is for the microphone. Internal controls on the amplifier/processor are often available to alter the frequency response and spread of volume control available to the user. Some analogue aids can now be digitally programmed to alter their processing performance. 2. Digital signal processing. Digital is best defined as sound that is represented mathematically. When digital signal processing (DSP) is used, the acoustic signal is converted to its electrical analogue at the microphone stage of the hearing aid system. After this conversion, a frequency filter is introduced to reduce

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possible distortion of the input signal, which is then sampled a defined number of times per second (normally, 10 000 times per second or greater). The analogue signal is then converted to its digital equivalent at the analogue to digital stage (A/D). Each of the samples receives a digital code. Binary numbers (0 and 1) are used to represent the digital value of each sample. Following the digitization of the signal, the digital representations are processed by a central processing unit (CPU) or microprocessor. The digital values can be multiplied, divided, added, subtracted and grouped in defined ways. In the microprocessor are various algorithms. For example, one algorithm may control the frequency response of the instrument, another may control loudness growth, a third may function to enhance the speech signal in a background of noise, etc. After the microprocessor has performed its tasks, the digitized signal must be converted back to its analogue equivalent. This is accomplished at the digital to analogue conversion stage (D/A). It is then again frequency filtered and amplified in the conventional manner and submitted to the ‘loud-speaker’ of the hearing aid. The obvious advantage of digital signal processing is that there are unlimited ways in which the signal can be manipulated. The numbers of parameters that can be utilized are significantly greater than those found in conventional analogue systems. As such, the ability to manipulate the signal to the acoustic needs of the patient is greatly enhanced, and this without excessive battery current demands. Types of aid As things currently stand most NHS aids are analogue in design. However the government have recently announced a ‘Beacon Site project’ to look at the logistics and feasibility of providing digital hearing aids through the NHS. Most digital aids are the same basic design as NHS aids, but as the DSP ‘chip’ is so much smaller than the corresponding analogue circuit they tend to be smaller and are often ‘in the ear’ (ITE) or even ‘in the canal’ (ITC) aids. 1. Postaural aids. In most common usage are the standard behind-the-ear (BEHA) aids, available on the NHS. The body of the aid sits behind the wearer’s ear and is normally connected by a hollow plastic tube to an ear mould, which allows sound passage to the ear. There are three main groups of BE aids, the 10, 30 and 50 series, with the power of the aids increasing correspondingly. Within each series are a number of models with differing patterns of frequency response. All contain an induction coil which can be used with telephones, televisions and in theatres and cinemas, fitted with induction loops, to bypass much of the unwanted back-ground noise. 2. ITE or ITC aids. These commonly available commercial aids sit in the concha or canal. Their external shell is usually of acrylic and conforms to the shape of the wearer’s ear. They are less obtrusive than the standard BE aids but are expensive and occasionally prone to feedback problems due to the proximity of microphone and ‘speaker’. 3. Body-worn (BW) aids. These rather cumbersome, ugly aids are usually worn with a strap around the neck and the body of the aid on the patient’s chest. By virtue of their size they can be made very powerful, and the distance between microphone and earphone means that, even with high amplification, feedback is rarely a problem. They are, however, prone to picking up the sounds of rustling clothes. There are two series available on the NHS: BW 60 and BW 80. 4. Bone conduction aids. These are very similar to the standard body-worn aid but feed their output to a bone conductor rather than an earphone. They are indicated because of meatal discharge or stenosis, or subjective preference for bone conduction reception. 5. Osseointegrated hearing aids. Conventional bone conduction aids have drawbacks, such as bulkiness and discomfort. In addition, the skull cannot be vibrated directly, but only through the energy-absorbing

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skin and soft tissues. Bone-anchored hearing aids largely overcome these problems. There are two devices in clinical use, both relying on the transmission of mechanical vibrations to the bone of the skull. (a) In the bone-anchored hearing aid (BAHA) a percutaneous titanium abutment is fixed to a titanium screw implanted in the mastoid. A vibrator is then mounted directly on to the abutment, which is fed either from a microphone and circuit in a small box with the vibrator or from a body-worn hearing aid (for higher output power). (b) The Xomed audiant bone conductor consists of an encased rare earth magnet implanted completely under the skin and fixed into bone with a titanium screw. Externally, another magnet serves to hold its surrounding induction coil in place over the implanted magnet. By passing electric currents (derived from what is essentially a hearing aid) through the induction coil, an electromagnetic field is set up that causes the implanted magnet, and hence the skull, to vibrate. 6. Implantable middle ear aids. The Symphonix sound bridge works on a similar principle to the Xomed audiant except that the external magnet vibrates a coil that is attached to the patient’s incus, thus directly vibrating the ossicles. 7. Spectacle aids. These involve modification of standard spectacle frames to incorporate a hearing aid. They can then be used in a number of ways: as a standard hearing aid, as a bone conductor or for contralateral routing of signal (CROS). In this last variation, sound is picked up from one side of the head and fed to the contralateral side, which is often the good side. Choice of aid Many factors will influence the choice of hearing aid. The actual degree and nature of the hearing loss will dictate the amplification characteristics. The cause of the deafness will influence the type of aid chosen, as will vanity and available finance. It is important to establish the patient’s requirements and to remember that an aid will not cure the underlying disease. 1. Type. A spectacle-type aid is useful for those people who regularly wear glasses as they are relatively inconspicuous. They are often chosen when there is one very deaf ear and a requirement for contralateral signal routing. A bone conduction aid is ideal in those cases where a hearing loss exists in association with active outer- or middle-ear inflammatory pathology. A body-worn aid is useful for anyone with a profound hearing loss. For most NHS patients an ear-level aid will be found to be suitable. 2. Amplification characteristics. The pattern of frequency response chosen depends very much on the shape of the audiogram. As for amplification, a hearing aid must function in a relatively narrow dynamic range, providing adequate amplification to overcome the hearing loss, but not over-amplifying sound and causing recruitment and consequent discomfort and intolerance. In an effort to overcome this problem, a number of formulae have been developed to calculate the appropriate amplification for the patient’s hearing loss (half-gain rule, Berger’s procedure, POGO 2, NAL-R, etc.). All formulae give differing importance to differing frequencies, with maximum importance for hearing loss at the main speech frequencies of 1000 and 2000 Hz. Many patients with deafness have a high frequency loss with comparative sparing of the lower frequencies. Most hearing aids can be adjusted to alter their frequency response, for instance high tone boost and base tone cut. More flexibility exists with digital signal processing. 3. Ear moulds. A number of modifications can be made to the ear mould. These may be made for both auditory and medical reasons. Venting the mould will reduce the low-frequency response. In patients prone

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to otitis externa, it is useful to ventilate or even skeletonize the mould to provide aeration. Unfortunately, feedback becomes more likely with a high-power aid if the mould is vented. 4. General. Although it is preferable to provide binaural aids in cases of bilateral hearing loss, this is rarely possible in the NHS on the grounds of cost, although the National Institute for Clinical Excellence (NICE) have recently endorsed this approach. Which ear to fit the aid in will then depend on a number of factors, including patient preference, available dynamic range and discrimination scores in each ear. The presence of any active inflammatory process in either ear, as well as other medical factors such as manual dexterity relating to arthritis, strokes, amputations, etc. also have a bearing. Follow-up and aftercare After the initial fitting, a period of support and rehabilitation is essential to allow the patient to gain confidence, iron out early teething troubles and achieve useful function with the hearing aid. In fact some would argue that this process is more important than the aid itself. Further reading
Ballantyne D. Handbook of audiological techniques. London: Butterworth-Heinemann, 1990. The Hearing Aid revolution. ENT News, Jan/Feb 2000, Volume 8(6). National Institute for Clinical Excellence. Technology appraisal guidance No. 8. Guidance on hearing aid technology, July 2000.

Related topics of interest Noise-induced hearing loss, p. 192; Presbyacusis, p. 252; Otosclerosis, p. 223; Pure tone audio-gram, p. 254.

HIV INFECTION

Aetiology Acquired immunodeficiency syndrome (AIDS) is caused by two of five human retroviruses: human immunodeficiency viruses (HIV) 1 and 2. (The other three are T-cell leukaemia viruses and are associated with lymphomas and leukaemias.) Pathology HIV-l is prevalent worldwide, while HIV-2 is found mainly in west Africa. HIV infects cells bearing the CD4 antigen, which acts as a virus receptor. Such cells are monocytes, macrophages and T-helper cells. The HIV-1 glycoprotein, gp120, binds to CD4 and allows the virus to enter the cell. Viral replication may occur in cells in which HIV-1 DNA has been integrated (productive infection), although in some cells containing integrated HIV-1 DNA, the virus does not replicate except when the cell is activated by antigenic stimulation (latent infection), for example by Epstein-Barr virus or cytomegalovirus infection. Ultimately, a functional impairment and depletion of T-helper cells occurs, but to a degree that is disproportionate to the number of cells infected. The mechanism of this has yet to be elucidated, but may relate to damage to lymph node architecture. The ultimate consequence is a compromise of the host immune system. Immunosuppression places the victim at risk of developing opportunistic infections and unusual malignancies, particularly B-cell lymphoma and Kaposi’s sarcoma. Clinical features AIDS is defined as the development of a complication of immunosuppression such as malignancy or opportunistic infection in an HIV-positive individual. The CD4+ T-cell count will be less than 200/mm3. Although the time to development of AIDS is variable, the majority of infected individuals in developed countries will develop AIDS about 10–11 years after infection with HIV, in the absence of treatment. So far only about 2% of infected individuals have avoided progression to AIDS. It is invariably fatal, with nearly two-thirds of reported sufferers in the USA already dead. There are various methods of transmission, but all demand close contact with infected body fluids, particularly blood. High-risk groups include intravenous drug users, homosexual males, heterosexual contact with an infected partner and children of infected mothers. Although transfusion of blood products, particularly in haemophiliacs, resulted in a significant number of cases, the screening of all blood products for HIV-1 and HIV-2 antibody has greatly reduced but

are usually between the ages of 20 and 40. The occurrence of unusual organisms requires a high index of suspicion to make the diagnosis followed by appropriate therapy. e. 4. Management The management of HIV infection as it presents to the ENT surgeon and the management of the patient so as to avoid the risks of infection pose separate problems. radiology) are dictated by the clinical conditions. Plasma HIV RNA assays give useful information when measured sequentially about both disease progression and response to anti-viral treatment. Neoplastic lesions are confirmed histologically on biopsy. atypical mycobacteria. Kaposi’s sarcoma and lymphomas may be found in the nasopharynx. 2. .HIV INFECTION 123 not irradicated the risk because it may take up to 4 months for seroconversion (the interval between infection and the appearance of antibody). using first an enzyme-linked immunosorbent assay (ELISA) as a screen. Radiotherapy and chemotherapy may be used for Kaposi’s sarcoma and lymphomas. Acute sinus infections may occur and unusual organisms such as yeasts and fungi are not uncommon. The oral cavity is one of the most commonly affected sites. Rhinological. Kaposi’s sarcoma is not uncommon. followed by western blot confirmation. anaemia and diarrhoea. two sets of common sense recommendations have developed. AIDS-related complex (ARC) comprises persistent fever lasting longer than 3 months. Severe candidiasis is frequent and may spread to involve the pharynx and larynx. Otitis media and externa (particularly fungal) are more common. Oropharyngeal. weight loss.g. They often culture unusual organisms. Herpes simplex ulceration is also common and tends to be widespread and severe. Usually this is done by identifying a specific antibody.g. excluding children. Monitoring of the CD4+ T-cell count is helpful as a surrogate measure of immune function. ENT disorders and HIV infection Between 40 and 70% of patients will have head and neck manifestations. Chronic rhinosinusitis may occur because of the debilitated state of the patient. Generalized cervical lymphadenopathy is a frequent finding in all AIDS patients. Other investigations (e. leucopenia. To reduce this risk. Xerostomia is a frequent complaint and epiglottitis is reported to occur more often. Kaposi’s sarcoma of the pinna or external auditory meatus may occur. Salivary glands may enlarge. 3. Investigations The diagnosis of HIV infection depends on detecting the virus or the host response to it in the blood. Typical patients are in one of the high-risk groups and. Opportunistic infections are diagnosed by appropriate sampling and microbiological culturing. Neck abscess may occur and tend to be deep. The CD4+ T-cell count is less than 400/mm3. AIDS patients are prone to a variety of conditions: 1. Risk of infection The risk of infection to a health care worker from an HIV-positive patient is extremely low and invariably relates to blood exposure. Neck. Otological.

Joint Working Party of the Hospital Infection Society and Surgical Infection Study Group. combination therapy may be used. Sinusitus. p. • Theatre precautions apply to any invasive procedure on a proven or suspected HIV-positive patient. 1992. British Medical Journal.124 OTOLARYNGOLOGY • Universal precautions should be adopted for all patients and involve the use of gowns and gloves to avoid blood contamination. Halitosis. and for other HIV infected individuals. 1991. but the theatre should be thoroughly cleaned with hypochlorite solution prior to the next case. p. There is no evidence of infection risk from the anaesthetic system. 1992. Further reading Gold JWM. 115. p. Otolaryngologic aspects of the acquired immunodeficiency syndrome. 305:1337–1343. Drapes should be disposable and double bagged at the end of the procedure. 76:1–18. 75:1389–1399. Non-Nucleoside (NNRTI) and Nucleoside Analogue (NARTI) Reverse Transcriptase Inhibitors. The General Medical Council recommends that a HIV-positive clinician should not perform invasive procedures. 29. 209. All staff should be fully gowned and double gloved and boots and eye protection should be worn. 271. p. Lucente FE. Appropriate serological monitoring is then required over a period of several months. . Follow-up and aftercare In general terms these patients are best cared for in a centre with a team with a particular interest in AIDS. Salivary gland diseases. Should inoculation occur. but sensible hygienic measures should be employed. Related topics of interest Cervical lymphadenopathy. p. Risk to surgeons and patients from HIV and hepatitis: guidelines on precautions and management of exposure to blood or body fluids. HIV-1 infection: diagnosis and management. Medical Clinics of North America. A high level of discipline is required in these cases. Current effective antiviral agents include Protease Inhibitors (PI). The patient need not be last on the list. The most senior or experienced surgeon/clinician should operate and theatre/ancillary staff should be kept to a minimum. Generally ‘triple’ therapy is recommended to avoid drug resistance in a very similar fashion to treatment of tuberculosis. Otitis externa. All non-intact skin surfaces should be covered and sharps should be handled with appropriate caution. 285. Medical Clinics of North America.

More than 10% of patients have a second tumour in the oesophagus. Tumours of the lateral wall of the piriform fossa may invade the thyrohyoid membrane and present as a palpable neck mass which may represent direct extension of the tumour rather than an enlarged lymph node. This extends from the pharyngoepiglottic fold to the opening of the oesophagus. with postcricoid carcinoma (30%) and posterior pharyngeal wall tumours (10%) occurring less often. In the postcricoid site the reverse is true. Extends from the level of the arytenoid cartilages and connecting folds to the inferior margin of the cricoid cartilage.HYPOPHARYNGEAL CARCINOMA The hypopharynx extends from the lower limit of the oropharynx at the level of the hyoid bone down to the lower level of the cricoid cartilage at the opening of the oesophagus. 3. It is bounded medially by the aryepiglottic folds and laterally by the inner surface of the thyroid cartilage. but the piriform fossa (60%) is the most common site. Medial wall tumours invade the aryepiglottic fold and into the paraglottic space. It is a disease of the elderly and the incidence is higher in men than in women. A few patients who had irradiation for thyrotoxicosis many years ago are now presenting with pharyngeal carcinoma after a latent period of 25–30 years. Pathology More than 90% of tumours of the hypopharynx are squamous cell carcinoma. Carcinoma of the hypopharynx in itself is an uncommon disease with a prevalence of less than 1 per 100 000 population. whereas an ulcerated lesion is typical of the other parts of the hypopharynx. Posterior pharyngeal wall Extends from the level of the floor of the vallecula to the level of the inferior border of the cricoid cartilage. For the purposes of tumour classification the UICC recognizes three anatomical sites: 1. Tumours of the posterior pharyngeal wall and the upper piriform fossa tend to be exophytic. Other epithelial and mesodermal tumours of benign and malignant behaviour do occur. 2. causing fixation of the vocal cord and consequent hoarseness. Hypopharyngeal tumours also have a propensity to metastasize to cervical . Piriform fossa. but they are rare. Approximately 2% of patients with the Paterson-Kelly-Brown syndrome (iron deficiency anaemia. Dissemination of hypopharyngeal tumours in the submucosal lymphatics leads to a high incidence of ‘skip lesions’. angular stomatitis. thus forming the anterior wall of the hypopharynx. the association is not as clear as with other upper aerodigestive tract tumours. Hypopharyngeal tumours are sometimes so advanced when first seen that it is difficult to determine the site of origin. koilonychia and splenomegaly) will develop postcricoid carcinoma. glossitis. pharyngeal web. Postcricoid (The pharyngo-oesophageal junction). Although tobacco smoking and alcohol have been implicated as aetiological agents.

Radiography. at first for solids then for fluids. Management of the patient will depend on. A full blood count to exclude anaemia and biochemical tests are required as electrolyte disturbances are not infrequent. Laboratory tests. 3. and more than two-thirds of these patients will have lymph node metastases at presentation. the site and extent of the disease. Hoarseness may occur as a result of invasion of the larynx or vocal cord paralysis. There may be vocal cord fixation. A soft-tissue neck radiograph is of limited value. particularly its upper and lower limits. and/or oesophagus. The piriform fossa has the richest lymphatic drainage. Investigations 1. but it may show a shadow posterior to the trachea. This allows staging of the tumour and a representative biopsy to be taken. T3 Tumour measures more than 4 cm in greatest dimension. The neck must be examined for lymph node metastases. Clinical features Early symptoms include the sensation of a lump or discomfort in the throat. 2. Later the patient will usually present with dysphagia. or measures 2–4 cm in greatest dimension. Direct laryngoscopy and oesophagoscopy should be performed in every patient who has an abnormal barium swallow or persistent symptoms despite a normal barium swallow. Digital examination of the tumour is appropriate if there is superior spread. with half of these being bilateral. Postcricoid tumours have a tendency to spread to paratracheal nodes. thyroid/cricoid cartilage. This can be regarded as abnormal if it is wider than the thickness of a vertebral body. prevertebral fascia. Bronchoscopy should be performed to look for any spread to the trachea. . or with fixation of the hemilarynx. TNM Stage T1 Tumour limited to one subsite of hypopharynx and 2 cm or less in greatest dimension T2 Tumour invades more than one subsite of hypopharynx or an adjacent site. which will usually demonstrate the presence and extent of any hypopharyngeal tumour or oesophageal lesion. Indirect laryngoscopy may reveal an obvious tumour or oedema of the arytenoids with pooling of saliva in the piriform fossa. A chest radiograph is mandatory to exclude metastases and to demonstrate any consolidation due to aspiration.126 OTOLARYNGOLOGY lymph nodes. among other factors. The extent of the lesion. Laryngeal crepitus is lost in post-cricoid tumours and occasionally a direct extension of the tumour through the thyrohyoid membrane is palpable. and all patients should have their necks palpated again while they are under the general anaesthetic.g. MRI is preferable to CT scanning in delineating the extent and spread of tumour. Endoscopy. T4 Tumour invades adjacent structures e. neck soft tissues. Every patient who presents with swallowing difficulty or the sensation of a lump in the throat should have a barium swallow. need to be assessed. The patient with advanced disease may have anorexia and weight loss. There may be a history of food sticking and repeated aspirations which will cause pneumonia.

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Management Hypopharyngeal carcinoma generally has a poor prognosis even with extensive surgery, and 60% of patients are dead within a year of diagnosis. Because of the low survival and high recurrence rate the choice of treatment is particularly important. The optimal treatment modality should provide the best chance of cure, the lowest mortality and morbidity, the shortest hospital stay and the highest chance of good upper aerodigestive tract function (speech and swallowing). All patients should have some treatment to their neck. In patients with an NO neck the overall risk of occult nodal metastases may be as high as 40–60%. Bilateral nodal involvement is common. Therefore treatment of both sides of the neck and the retropharyngeal lymph nodes with either surgery or radiotherapy must be considered electively. Metastases are most common in levels II, III and IV. A lateral selective neck dissection is therefore appropriate if surgery is the preferred modality. Treatment may consist of radiotherapy, surgical resection, combined therapy or palliative therapy. 1. Radiotherapy. Early hypopharyngeal cancer may be treated with radiotherapy, with the option of salvage surgery if there is a recurrence. Radiotherapy may be reserved for the patient without enlarged lymph nodes, but it has been proposed that in selected cases radiotherapy can be given to the primary tumour and a radical neck dissection carried out for nodal metastases. 2. Surgery. Surgical resection is preferred for large tumours or in the presence of bulky cervical metastases. A lateral pharyngotomy can be performed for posterior wall tumours and the defect repaired with a radial forearm free flap. Extensive and circumferential lesions will require total pharyngolaryngectomy and then reconstruction of the residual defect. A variety of techniques to reconstruct have been used including skin grafts, cervical and deltopectoral skin flaps, myocutaneous pectoralis major and latissimus dorsi flaps and visceral interposition of stomach, jejunum or colon. The main complications are failure of the graft or flap, postoperative fistulae and stenosis, which are all more likely if there has been previous radiotherapy. There is also a significant mortality rate of 1% for skin flaps and revascularized loops and up to 10% for gastric transposition. The choice of reconstruction depends largely on the experience of the unit. 3. Combined therapy. Postoperative radiotherapy is carried out within 6 weeks of surgical resection as a combined treatment, with the aims of destroying metastases and maximizing the recurrence-free life interval. It is indicated if: surgical resection margins are close to or involved in tumour, in most large tumours requiring surgery, when there is vascular or perineural invasion, more than 2 lymph nodes are involved, or if there is extra-capsular rupture. 4. Palliation. This therapy is for those patients with advanced end-stage disease, severe intercurrent illness, poor general condition, distant metastases, or those who refuse treatment. Palliative radiotherapy can be offered to produce tumour shrink-age and symptom relief in some cases. Follow-up and aftercare On the 10th postoperative day, if there is no evidence of graft failure or leak, the patient can be tested with a methylene blue or gastrograffin swallow. If there is no evidence of extravasation, the patient can be commenced on fluids and then soft diet. Most patients will require thyroid, calcium and calciferol replacement for life. Speech rehabilitation is difficult in these patients, although there are some encouraging reports with low-pressure speech valves (e.g. Provox or Blom-Singer), the voice is not as good as after a total laryngectomy. Patients should be regularly reviewed in the clinic and their nutritional status and swallowing ability should be monitored along with a careful examination for primary and secondary recurrence.

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Further reading
Jones AS, Roland NJ, Husband D and Gati I. Free revascularised jejunal loop repair following total pharyngectomy for carcinoma of the hypopharynx, a report of 90 cases. British Journal of Surgery, 1996; 83:1279–1283. Schetter GL. Cancer of the hypopharynx and cervical oesophagus. Current Opinion in Otolaryngology and Head and Neck Surgery, 1998; 6:97–101. Wilson J (ed). Effective Head and Neck Cancer Management. Second Consensus. British Association of Otolaryngologists, Head and Neck Surgeons, 2000.

Related topics of interest Globus pharyngeus, p. 113; Laryngeal carcinoma, p. 138; Oral cavity carcinoma, p. 197; Oropharyngeal carcinoma, p. 203.

IMPEDANCE AUDIOMETRY

Physics and physiology The middle-ear and mastoid air cells communicate with the nasopharynx via the Eustachian tube. As a closed system, air is being continually absorbed by the lining mucosa but is periodically replaced when the Eustachian tube opens, during the act of swallowing. Sound transmission from the external to the inner ear is optimal when the compliance of the middle-ear system is maximal, i.e. when the pressure in the middle ear is equal to the pressure in the external auditory meatus. Compliance (or admittance) is the measure of this system to allow the passage of sound energy through it, and is inversely related to impedance, which is the resistance to the passage of sound energy. The mass, stiffness and frictional resistance of the medium through which the sound wave travels contribute to the impedance, which at low frequency is stiffness dominated. Strictly speaking, compliance is the reciprocal of stiffness so that impedance measurements at low frequency are usually referred to as the compliance. Basic principles Impedance audiometry consists of three tests: tympanometry, acoustic reflex testing and static compliance. All three tests work on the same basic principle. The test probe consists of a sound producer, a sound receiver and a device for altering the air pressure within the EAM. The probe has a soft plastic or rubber tip to allow an air-tight seal in the EAM. A test tone is made (220 Hz, 65 dB) into the EAM, of which some will be absorbed (admitted) by the middle-ear system (drum and ossicles) and some reflected. The reflected sound energy is measured by the probe microphone. The compliance, that is the amount of sound absorbed by the middle-ear system, can be determined either by measuring the reflected sound level in the ear canal or more commonly by measuring the amount of energy required to keep the sound level constant at varying ear canal pressures. The compliance will be maximal when the ear canal pressure is equal to middle-ear pressure, that is when there is no pressure differential across the tympanic membrane. A tracing of the compliance as ear canal pressure alters allows this and other parameters to be determined. Clinical uses 1. Tympanometry. This test is the most commonly used aspect of impedance audiometry and is particularly useful in evaluating children with otitis media with effusion. Here compliance is measured continuously while the pressure in the EAM is automatically varied from +200 to -400 mm H2O. This gives a graphical result which can be classified into one of three groups:

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(a) Type A. Maximal compliance occurs when the pressure in the EAM is between +50 and -100 mm H2O. A normal maximal compliance value is between 2 and 4 ml. A low value for maximal compliance indicates stiffness of the middle-ear system as in tympanosclerosis or otosclerosis. A high or unrecordable peak of compliance indicates excess mobility of the middle-ear system as in ossicular discontinuity or atelectasis. (b) Type B. A low-value flat or horizontal compliance trace occurs, implying persistently low compliance. This is usually taken to indicate fluid in the middleear cavity, and in young children (< 7 years) with glue ear can be correlated with audiometric hearing loss. A type B tympanogram will also occur in the presence of a perforation in the tympanic membrane but the ear canal volume will be large (> 6 ml) because it is measuring that of the middle-ear cleft too. It can occasionally be useful in confirming this diagnosis or to test the patency of a ventilation tube. (c) Type C. This group give a peak compliance when the pressure in the EAM is < -100 mm H2O. This indicates a significant low pressure in the middle-ear system and is a sign of eustachian tube dysfunction. The C curve can be subdivided into Cl, when the peak is between -100 and -199 mm H2O, and C2, when the peak occurs at less than -200 mm H2O. 2. Acoustic reflex measurement. Acoustic reflexes are measured at the ear canal pressure producing maximum compliance, which corresponds to middle-ear pressure. Ipsilateral reflexes are recorded using the tympanometry probe; contralateral reflexes use a monaural headset to deliver sound to the non-probe ear. It is usual to test at 0.5 kHz and then at either 1 or 2 kHz. A sound intensity of 70–90 dB above the pure tone threshold at that frequency is required to elicit a reflex in a normal-hearing subject, although in one who has a recruiting sensorineural hearing loss a reflex may be present only 10 dB above threshold. The compliance, which is constant for the ear canal pressure selected, is recorded as a horizontal line and shows a dip on contraction of stapedius muscle, representing a reduction in compliance. The stapedial reflex is a complex crossed reflex and demands an intact afferent arm, brain stem and VIIth cranial nerve. As such, the acoustic reflex can provide diagnostic information with regard to the site of a neurological lesion based on the pattern of response to ipsi- and contralateral testing. It is important to remember that a conductive hearing loss of only 5 dB may result in an absent ipsilateral and contralateral (for reasons that have not been satisfactorily explained) reflex, although it is not until there is a 15 dB air-bone gap that the reflex is absent in 50% of cases. Adaption (stapedial reflex decay) is determined by producing a persistent tone in the test ear and measuring the reflex in the contralateral ear. Normal adaption occurs only after 10 seconds, decay being no more than 50%. Summary of the value of measuring the acoustic reflex: (a) Assesses the integrity of the facial nerve up to the branch to stapedius tendon. (b) Assesses recruitment and stapedial reflex decay, the latter in particular being an accurate pointer in distinguishing a cochlear (recruiting) from a retrocochlear (abnormal decay) lesion. (c) Assess the presence of a conductive hearing loss. (d) Assess brainstem function. 3. Static compliance. The least used of the three tests. The compliance is measured with an air pressure of +200 mm H2O in the EAM, and this figure is subtracted from the maximal compliance, regardless of the pressure in the EAM at which this occurs. The normal range for this is from 0.3–1.6 ml. A figure greater than 2.0 ml implies the presence of a tympanic membrane perforation.

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Conclusion Impedance audiometry is rapid and easy to use. It provides an objective measure of middle-ear function, can help to distinguish cochlear from retrocochlear hearing loss, as well as localizing brainstem and facial nerve lesions. It is, however, essential that the results are interpreted in the context of other clinical findings. Further reading
Ballantyne D. Handbook of Audiological Techniques. London: Butterworth-Heinemann, 1990. Jerger J, Hayes D. Clinical use of acoustic impedance testing in audiological diagnosis. In: Beagley HA (ed.) Audiology and Audiological Medicine, Oxford: Oxford University Press, 1981.

Related topics of interest Acoustic neuroma, p. 1; Clinical assessment of hearing, p. 45; Facial nerve palsy, p. 92; Otitis media with effusion, p. 213; Pure tone audiogram, p. 254; Speech audiometry, p. 301.

INTRINSIC RHINITIS

Intrinsic rhinitis (IR) is an inflammatory condition of the nasal mucosa which is probably better described by the title non-infective, non-allergic rhinitis. As such it represents, to some extent, a diagnosis of exclusion. Pathology IR has been divided into two types, eosinophilic and non-eosinophilic, on the basis of the numbers of eosinophils found in the nasal secretions. However, recent research evidence has cast doubt on this distinction. It is likely that the condition represents more than one pathological process. Upsets to the autonomic nervous system have been postulated, but it would appear that immunological abnormalities are common. Of particular recent interest has been the separate findings of anti-IgE antibodies and elevated nasal IgE levels. A number of patients demonstrate an intrinsic mucosal disorder of prostaglandin metabolism. In this type there is an association with aspirin hypersensitivity, asthma and nasal polyposis. Regardless of the underlying aetiology most patients demonstrate glandular hyperplasia and submucosal vascular dilation. The nasal mucosa becomes hyperaemic and hypertrophic, particularly on the turbinates. Eosinophil-laden polyps are more common in IR than in allergic rhinitis. Predisposing factors • • • • • • • • • Familial tendency. Preceding infection (nasal mucosal hyper-reactivity following viral or bacterial rhinitis). Psychological and emotional factors. Endocrine (puberty, menstruation and pregnancy). Drugs (hypotensive agents, e.g. beta blockers and methyl dopa, aspirin, oral contraceptives). Pollution (atmospheric pollution, fumes, dust, industrial detergents and cigarette smoke). Atmospheric conditions (changes in humidity and temperature). Alcohol. Smoking. Clinical features IR accounts for 40–70% of all cases of perennial rhinitis and becomes more common with increasing age. All patients exhibit nasal obstruction and rhinorrhoea or post-nasal discharge, but itching and sneezing are less common than in allergic rhinitis. Patients vary in their degree of nasal obstruction and discharge. There may

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be associated nasal polyps with anosmia. Co-existent sinus pathology is frequently found (up to 50%) which may be primary, causing a secondary rhinitis, or secondary due to the inevitable compromise of sinus aeration and drainage. Examination generally reveals a rather red and angry mucosa, often with copious secretions and hypertrophy of both middle and inferior turbinates, causing a consequent reduction in the airway size. Investigations IR is a diagnosis of exclusion, and the aim of investigations is to identify other causes of rhinitis. IgE estimation by PRIST and RAST and skin testing can be used to indicate allergy. Radiological examination of the nose and sinuses with CT scanning may help diagnose structural abnormalities and any coexistent sinus infection. Management 1. Medical. Antibiotics may be used to treat any co-existent infective component and a short course of oral steroids is often helpful to get an initial response. However the mainstays of maintenance treatment are as follows: (a) Intranasal steroids. Many cases respond well to topical intranasal steroid preparations although in some the response is disappointing. (b) Antihistamines are useful in some cases. Older preparations such as chlorpheniramine have anticholinergic effects and are to be preferred but sedative side-effects may be troublesome. Topical preparations can sometimes have an impressive local effect. (c) Topical ipratropium bromide is useful for its anticholinergic effect in reducing rhinorrhoea. (d) Systemic sympathomimetics can be helpful (e.g. pseudoephedrine), though they may produce unpleasant side-effects such as dry mouth, constipation and excitability. They should not be used long term or in children. (e) Local nasal decongestants. Self-medication with topical vasoconstrictors (e.g. xylometazoline, ephedrine) is common and initially successful in bringing relief to the patient with enlarged turbinates by reducing blood flow in them. Unfortunately, when the effects wear off, there is a reflex vasodilatation causing increased blood flow and turbinate engorgement (rebound phenomenon). Prolonged use leads to an aggravation of symptoms, which eventually become unre-sponsive to the decongestant, and rhinitis medicamentosa may supervene. The treatment is to stop the decongestant and prescribe topical nasal steroids. (f) Interleukin antagonists. Although not yet established in the management of this condition, it is likely that developments in this area will ultimately prove helpful. Some clinicians are already using them on a limited basis and with some success. 2. Surgical. Surgical treatment is useful for the control of symptoms, particularly nasal obstruction, when medical treatment is ineffective. (a) Treatment of concomitant problems. Associated nasal polyps are treated with excision or topical intranasal steroids as appropriate. Correction of septal deflections and spurs should be considered to relieve an obstructed airway.

108. Partial resection of the middle turbinate at functional endoscopic sinus surgery. p. Idiopathic rhinitis: idiopathic or not? Clinical Otolaryngology. Lancer JM. Journal of the Royal Army Medical Corps. Banfield GK and McCombe AW. laser cautery. 174. Further reading Jones AS. but obstruction recurs after 1–2 years. Related topics of interest Allergic rhinitis. linear diathermy. 1999. Initial enthusiasm for Vidian neurectomy for the relief of rhinorrhoea without nasal obstruction waned when it became apparent that over 50% of patients relapsed within 1 year. Vasomotor rhinitis (editorial). 21:198–202. 84. Functional endoscopic sinus surgery. Nasal polyps. The theoretical risk of atrophic rhinitis has not materialized in UK practice. There is no doubt that any associated sinus disease can be addressed with FESS. This operation divides the parasympathetic nerve supply to the nose as the nerve of the pterygoid canal (Vidian nerve) enters the pterygopalatine fossa. Submucosal diathermy. 145:18–19. Carney AS and Jones NS.134 OTOLARYNGOLOGY (b) Turbinate surgery. p. Examination of the nose. p. Most procedures are aimed at reducing the bulk of the inferior turbinate to improve the airway. Inferior turbinectomy is associated with slightly higher morbidity from postoperative haemorrhage but is more successful for long-term symptom control. . 1996. (c) Vidian neurectomy. cryosurgery and multiple outfractures are all successful in the short term. Some clinicians will also trim the middle turbinates in this procedure to achieve significant improvements in the nasal airway. 294:1505–1506. 11. p. (d) Functional Endoscopic Sinus Surgery (FESS). British Medical Journal 1987.

Three important definitions are provided to aid their understanding. For example . perilabyrinthitis and paralabyrinthitis. The mechanism is pressure transmission to the labyrinth causing endolymph movement and stimulation of the labyrinthine sense organs. Labyrinthine fistula A labyrinthine fistula is a bony erosion of the labyrinthine capsule to expose. A breach will usually result in a dead ear. but not breach. the endosteum of the labyrinth. but silent. Tullio phenomenon The Tullio phenomenon is defined as vertigo in the presence of loud sounds. Releasing the pressure allows the deviated eyes to return to the midline. A fistula most commonly occurs in the dome of the lateral semicircular canal. On occasion it may occur by a similar mechanism to the Tullio phenomenon. raising the ear canal pressure of the affected side may cause conjugate deviation of the eyes away from the affected ear. The fistula may have been present. this scenario arising in the 1950s in patients with severe adhesive otitis. The phenomenon occurs when sound energy is transmitted from a mobile stapes foot-plate to the labyrinth which is distensible only when there is a fistula. The phenomenon may also arise in those with endolymphatic hydrops when it is thought to be secondary to sound energy transmission from the footplate to the distended saccule which may be touching the undersurface of the footplate in advanced cases. The fistula sign In the presence of a labyrinthine fistula. Perilabyrinthitis Perilabyrinthitis is a syndrome caused by a labyrinthine fistula after mastoid surgery in the presence of retained labyrinthine function.LABYRINTHITIS Labyrinthitis is an inflammation of the labyrinth and may be classified into serous labyrinthitis. suppurative labyrinthitis. Historically the phenomenon occurred if a fenestration procedure was performed in the presence of a mobile footplate. This occurs either directly if there is labyrinth endosteum exposed to the ear canal after mastoid surgery or indirectly if endosteum is covered by disease that can transmit the pressure wave such as cholesteatoma. before surgery.

Here the symptoms and signs are different. that is nystagmus in any direction of lateral gaze. This can be understood when we explain the normal labyrinth causes conjugate deviation of the eyes to the opposite side so that if one labyrinth is paralysed the opposite labyrinth will become dominant and deviate the eyes to the side of the affected ear. Alternatively the fistula may be iatrogenic. sealing the graft with fibrin glue and a temporalis muscle flap. Investigations of labyrinthitis The diagnosis is made on the clinical features occurring in the presence of a precipitating factor. In parallel with these changes is an improvement in mobility and symptoms. reducing the drive from the unaffected ear so that the corrective nystagmus and therefore the vertigo will be less severe. Paralabyrinthitis This is vertigo occurring in the presence of CSOM when inflammation close to the endosteum of the labyrinth causes an irritative nystagmus. Treatment consists of occluding the meatus with cotton wool when outdoors or grafting the fistula with temporalis fascia. Finally there is absence of nystagmus on optic fixation. The symptoms and signs are identical to suppurative labyrinthitis except in the latter the loss of inner ear function is irreversible. Tiny movements of the head exacerbate the vertigo so that the patient prefers to lie completely still on his side and in the presence of a paralytic nystagmus the affected ear will be uppermost. the nystagmus occurring as a corrective measure. that is a nystagmus towards the affected ear. The ears should always be examined under the microscope and if any debris is found it should be removed. Serous and suppurative labyrinthitis Serous labyrinthitis is a retrospective diagnosis and depends on there being some recovery of cochlea and vestibular function after an attack of postulated bacterial labyrinthitis. but may be difficult to recognize . the mass of the cholesteatoma sac prevents distension of the labyrinthine endosteum. As compensation gradually occurs second degree nystagmus develops (nystagmus when gazing straight ahead or looking in the direction of the nystagmus) and then first degree nystagmus (nystagmus only when looking in the direction of the nystagmus).136 OTOLARYNGOLOGY when secondary to cholesteatoma. Initially there is third degree nystagmus. Vertigo may also arise in perilabyrinthitis on windy days when the relatively cooler wind produces a thermal gradient across the labyrinth and a difference in the specific gravity of endolymph at each end of the semicircular canal to cause circulation of the endolymph within the canal. or may also be a complication of ASOM via the round window. The hallmarks of perilabyrinthitis are the Tullio phenomenon and a positive fistula sign. A labyrinthine fistula may be visible. There may be a short period of irritative jerk nystagmus towards the affected ear. Clinical features Labyrinthitis is most commonly virally induced but may be secondary to CSOM. Typically. In this position the patient will tend to voluntarily look in the direction of the affected side (especially when they have visitors). If there are no features to suggest a meningitis the important diagnosis not to miss is a cerebellar abscess. there is an acute onset of violent. but soon a paralytic jerk nystagmus to the healthy ear ensues. overwhelming vertigo that is so severe it inhibits the perception of tinnitus and hearing loss.

.LABYRINTHITIS 137 in a patient continuously vomiting. Neurotrophic factors and antioxidants may therefore have a significant future role to play in the protection and recovery of inner ear receptors from injury of any aetiology. Cooksey-Cawthorne exercises may accelerate central compensation. Cochlea hair cells are more susceptible to injury than vestibular receptors which suggests the latter receptors should respond well to such attempted rescue and further work is on going. • Vestibular sedatives. using a herpes simplex virus (HSV) vector has been injected into the cochlea of mice whose hair cells had been killed with neomycin which allowed a near total rescue of cells within 4 weeks. Follow up and aftercare • After recovery from the acute infection. • An ear culture swab if there is evidence of middle ear infection and appropriate antibiotics. Future advances Growth factors and antioxidant cocktails may provide protection to the labyrinth from progressive damage and may allow regeneration of vestibular receptors. Osmotic pump infusion and viral vector delivery of GDNF into perilymph has attenuated kanamycin and ethacrynic acid sensory cell loss. • If the precipitating factor was CSOM. A labyrinthine fistula may have arisen from chronic osteitis or cholesteatoma. Management of labyrinthitis Treatment of both the precipitating factor and the labyrinthitis is necessary. The chronic disease should be eradicated and if a fistula is identified the treatment is described above. • Counselling is a necessary but often overlooked part of the management. Antioxidants will reduce sensory hair cell loss due to cisplatin and the protective function of antioxidants to gentamicin ototoxicity and to acoustic trauma has also been demonstrated. exploration of the mastoid after recovery from the acute symptoms. Furthermore changes in BDNF expression following trauma are correlated with the degree of regeneration. avoiding head movements. broad spectrum until results of the swab are available. if they develop a severe illness (allows inhibition of central compensation) or if they should develop a neuropathy affecting the peripheral proprioceptors. Even with complete central compensation patients with unilateral labyrinthine failure will still be unsteady in the dark. Sequential pure tone audiometry and electronystagmography (ENG) will allow the monitoring of recovery although hearing loss and vestibular failure is permanent with purulent labyrinthitis. • Intravenous fluids if vomiting. An enhanced CT or MRI scan will be necessary in these circumstances. • Bed rest. Growth factors of particular interest are brain-derived neurotrophic factor (BDNF) and glial cell line-derived neurotrophic factor (GDNF). The BDNF gene. should be considered.

Transforming growth factor alpha treatment alters intracellular calcium levels in hair cells and protects them from ototoxic damage in vitro. Acute suppurative otitis media. Chronic suppurative otitis media. Vestibular and balance rehabilitation therapy. p. Vestibular function tests. 1993. Telian SA. Int J Dev Neurosci. . 346. Malgrange B. 102:198–205. 1997. p. Raj A. p. 350. p. Vertigo. p. Rhinology and Laryngology. Staecker H.138 OTOLARYNGOLOGY Further reading Shepard NT. Dazert S. 38. 27. Smith-Wheelock M. Annals of Otology. 15:553–562. Related topics of interest Caloric tests. et al. 5.

Clinical features The clinical features of malignant disease are dictated by the primary tumour. In some areas of India and Malaysia it is the most common cancer and is probably related to variations in smoking habit. It extends from the apex of the laryngeal ventricle to 1 cm below. Glottis. Cough and irritation of the throat are occasional symptoms. The general symptoms of anorexia. The symptoms and signs of a laryngeal tumour depend on the way in which it is related to the upper aerodigestive tract. respectively. Patients with a cancer in this site may complain of a unilateral sore throat. The incidence increases with age. There may be referred otalgia. chondrosarcoma and lymphomas are all rare. but the peak age of presentation is in the seventh decade. arytenoids. aryepiglottic folds and the epiglottis (laryngeal surface. It is about five times commoner in males than in females. Some authorities hold that the superior and inferior borders of the glottis correspond to the superior and inferior arcuate lines. tip and lingual surface).LARYNGEAL CARCINOMA Pathology Squamous cell carcinoma of the larynx is the commonest head and neck cancer in the Western world and represents approximately 1% of all malignancies in men. Subglottis. Hoarseness is the commonest and often the only presenting symptom. Swelling of the neck may be due to direct penetration of the tumour outside the larynx or to lymph node metastases. 2. There should be a general examination to identify distant metastases and an assessment of the overall physical status of the patient. Dyspnoea and stridor are late symptoms and almost invariably indicate an advanced tumour. Supraglottis. 3. This comprises the larynx superior to the apex of the ventricle. vestibular folds. cachexia and fetor imply advanced disease. Dysphagia indicates invasion of the pharynx. It is very rare in non-smokers. Adenocarcinoma. Indirect laryngoscopy should allow an inspection of the primary tumour site . This comprises the vocal cords and the anterior and posterior commissures. It includes the ventricle. The cause of cancer of the larynx is not known. secondary deposits and the general effects of cancer. adenoid cystic carcinoma. fibrosarcoma. Alcohol on its own is probably not a cause of laryngeal cancer but it is highly synergistic with smoking. the larynx is divided into three regions which each include a number of sites: 1. For classification purposes. Verrucous carcinoma is a distinct variant of welldifferentiated squamous cell carcinoma. but persons who smoke tobacco and drink alcohol are predisposed to the disease. This extends from the inferior border of the glottis to the lower border of the cricoid cartilage. Pain is an uncommon symptom but is most typical in supraglottic tumours.

also undergo fibreoptic laryngoscopy. Supraglottis. but supraglottic tumours may cause bilateral nodes. Imaging may also uncover the presence of impalpable or occult nodes. mucosa of tongue base). An isotope bone scan is indicated only if symptoms suggest bony metastases or there is a raised serum calcium or alkaline phosphatase. Vocal cord mobility should also be assessed. therefore. An accurate anatomical description of tumour extent (with a case file diagram or photograph) is therefore essential in treatment selection. the patient should have a full panendoscopy including bronchoscopy. Direct laryngoscopy under general anaesthesia is mandatory. The chest radiograph should be carefully examined to exclude metastases or to assess intercurrent lung disease. While the patient’s neck muscles are relaxed under general anaesthetic the neck should be palpated for nodes which may not have been noted previously. All patients should. Investigations A chest radiograph. Biopsy material should include an adequate amount of representative tissue to obtain a definitive diagnosis of malignancy. and some subglottic tumours may spread to the upper mediastinal nodes. In addition. Examination must include an assessment of the number. A CT scan of the chest may be indicated if suspected lung metastases need further delineation. All the larynx sites should be inspected systematically. . and even with this standard there is considerable variability. neck or lung is in the region of 1–5%. Clinical staging attempts to group together features which may share a level of prognosis or a certain treatment. the laryngeal surface of the epiglottis and the laryngeal ventricle. mobility and level of the nodes.140 OTOLARYNGOLOGY and size. In cancer of the larynx. full blood count and serum analysis are baseline investigations prior to a general anaesthetic. Distant metastases are unusual in laryngeal carcinoma at presentation (1–5%). The serum analysis may show deranged liver function raising suspicion of liver metastases. T1 Tumour limited to one subsite of the supraglottis. There are three areas which are difficult to examine by this technique: the subglottis. The tumour’s position and extension should be recorded by means of a diagram in the case notes. clinical staging is the only generally reliable criterion of any prognostic significance. identification of the tumour type and tumour differentiation. or hypoproteinaemia. An ultrasound scan of the liver is required if hepatic metastases are suspected and in some units this is routine prior to major surgery.g. Staging Laryngeal tumours are diverse in their behaviour and prognosis and thus there have been many endeavors to classify them. Cord mobility should be assessed as the patient wakes if not done already. The information from the investigations of the patient allow the surgeon to ‘stage’ the tumour according to the TNM classification and manage it accordingly. Laryngeal tumours usually metastasize to the upper deep cervical lymph nodes. MRI or CT scans of the larynx and neck provide further information about the primary tumour. The neck should be carefully palpated for the presence of enlarged lymph nodes. T2 Invasion of more than one subsite of the supraglottis or glottis or adjacent region outside the supraglottis (e. The incidence of a synchronous second primary tumour in the head. which may indicate malnourishment and a possibility of poor wound healing.

. may be necessary. Extends beyond the larynx The presence of palpable lymph nodes is the most important factor in determining prognosis. small tumours are treated by radical radio-therapy in the first instance. Confined to the larynx with a fixed vocal cord. general condition. Some authorities maintain that transglottic tumours arise from the laryngeal ventricle. Tumour extends to supraglottis and/or subglottis. Glottis. Management of the neck will depend on nodal status (see Cervical Lymphadenopathy and Neck Dissection chapters). Involves both vocal cords. T4 Extends beyond the larynx. and a high proportion of these tumours spread to cervical lymph nodes. T1 (a) T1(b) T2 T3 T4 Tumour limited to one vocal cord. Larger tumours tend to be treated with primary surgery. N1 disease in cancers from all sites of the larynx can be treated by modified radical neck dissection and N2/N3 by radical neck dissection with a modified dissection on the contralateral side if required. Patients who present with stridor should have endoscopic debulking carried out when possible. but assessment of lymphadenopathy is subjective. with surgery reserved for recurrence. or impaired cord mobility. Extends beyond the larynx. surgery or a combination of these two modalities. Subglottis. The supraglottis has a rich lymphatic drainage. T1 T2 T3 T4 Tumour limited to subglottis. About one-third of patients with no palpable lymph nodes have histologically invaded nodes. Vocal cord fixed. usually with postoperative radiotherapy. Extends to vocal cords with normal or impaired mobility. Curative treatment may involve radiotherapy. although not desirable. epiglottic tissues. As a general rule. Tracheostomy.LARYNGEAL CARCINOMA 141 T3 Confined to larynx with a fixed vocal cord or invades the postcricoid area. Preservation laryngeal surgery is also an option with small tumours. base of tongue. 1. Supraglottic tumours have a high incidence of overt and occult nodal metastases and the NO neck needs elective treatment in these cases. Management Each patient will fall into one of the following treatment categories depending on their age. and a similar number of palpable nodes are not invaded by tumour. and stage of the tumour: curative treatment or palliative treatment. so metastases usually only occur when the tumour has spread to involve the supraglottis and subglottis in the so-called transglottic tumour. The subglottis drains to paratracheal and mediastinal nodes in addition to the cervical lymph node. The glottis has virtually no lymphatic drainage. Bilateral dissection of levels II-IV with inclusion of level I if tongue base involvement and level VI if subglottic spread.

Radiotherapy has the advantage of leaving the patient with his larynx. but its use is controversial. Subglottic tumours. palliative radiotherapy. approximately 50% of T3 laryngeal carcinomas are understaged and are in fact T4 tumours due to extension through the cricothyroid membrane or from unsuspected cartilage invasion. Small tumours may be treated by radiotherapy. but vertical partial laryngectomy is sometimes an alternative. . T1 In the UK. and have their weight recorded in the outpatient clinic on a regular basis. Early involvement of the palliative care team. sometimes as an emergency procedure. T1-T2 T3-T4 Usually treated by radiotherapy or conservation surgery. Follow-up and aftercare Patients who have had potentially curative treatment should be carefully examined for signs of primary recurrence. then 6 monthly for the next 3 years. every 3 months for 12 months. It is important that the upper mediastinum is included in the radical treatment regimen. Furthermore. combined with a neck dissection. small tumours confined to one vocal cord can be treated by endoscopic laser resection or open cordectomy. All patients should have had modern method of voice restoration following laryngectomy including valved speech. tracheostomy. Some units continue to monitor patients as the incidence of second primary tumours is in the region of 10–20%. T2 They can be similarly managed by radiotherapy or by partial laryngectomy. Glottic tumours. Alternatively. This should be monthly for the first 6 months. Radiotherapy may be better for extensive superficial tumours because of the better functional results obtained. Larger tumours causing stridor will need a total laryngectomy.142 OTOLARYNGOLOGY 2. Pure subglottic cancer is very unusual. but there is often persistent oedema. The results of salvage surgery for recurrences after radiotherapy are poor. Palliative treatment includes pain relief. The subglottis becomes involved in extensive glottic and transglottic carcinoma. radiotherapy has been the conventional treatment of choice for T1 glottic tumours. Patients who have had a laryngectomy will require speech therapy. T4 Tumours will be treated by total laryngectomy and a radical neck dissection if there are any nodal metastases with post-operative radiotherapy. Primary surgery with post-operative radiotherapy is therefore recommended for high volume lesions. but these tumours often present late and the patient needs a total laryngectomy. giving cure rates in excess of 90%. chemotherapy and occasionally surgery. Supraglottic tumours. insertion of a percutaneous gastrostomy. Larger tumours will require treatment by either a supraglottic laryngectomy or total laryngectomy. Endoscopic resection may have a role in selected T1 cases. T3 Many T3 glottic tumours are treated in the first instance by radiotherapy. sometimes with aspiration and poor function of the larynx. They will also require monitoring of their thyroid function and calcium levels if there has been a thyroid gland excision. neck node spread and distant metastases. then every 2 months for 6 months.

2000. 336. 1993. Review. 264. Cancer of the larynx.LARYNGEAL CARCINOMA 143 Further reading DeSanto LW. Laryngectomy. Tracheostomy. British Association of Otolaryngologists. Prognostic factors in laryngeal carcinoma. Second Consensus Document. 13:399–409. p. Radiotherapy. 185. Neck dissection. Related topics of interest Cervical lymphadenopathy. Effective Head and Neck Cancer Management. 143. Current Opinion in Otolaryngology and Head and Neck Surgery. p. Clinical Otolaryngology. . Wilson J (ed). p. 1:133–136. Stell PM. p. 1988. p. Head and Neck Surgeons. 29.

3.) are invariably treated by laryngectomy. verrucous carcinoma. the general health of the patient and the relative consequences of the treatment. Near-total laryngectomy. the main handicap associated with this procedure. Although patients may undergo speech rehabilitation and may swallow well after removal of the larynx. (a) Supracricoid partial laryngectomy. Types of laryngectomy 1. Radiotherapy has the advantage of vastly reduced morbidity compared with surgery. partial laryngectomy and surgical voice restoration. The repertoire must include conservation techniques including laser surgery. 2. With both a laryngectomy and radiotherapy there is invariably some or total loss of normal voice and compromise of airway protection and function. The goals of conservative laryngeal surgery are to control cancer and obtain a functional outcome of speech and swallowing without the need for a permanent tracheostomy. (a) Cordectomy. according to quality of life studies. In general in the UK. appears to be the need for a permanent stoma. It is apparent that the modern surgeon should not manage laryngeal cancer on the basis of one surgical option (total laryngectomy). Horizontal partial resection. The other less common malignant neoplasms of the larynx (adenocarcinoma. fibrosarcoma. etc.LARYNGECTOMY The choice between surgery and radiotherapy as treatment for carcinoma of the larynx should be made according to the likely effective control of the cancer. (b) Supraglottic laryngectomy. are popular in the USA and Continental Europe. lateral and fronto-lateral). . radiotherapy is reserved for smaller tumours (T1 and T2). Conservative approaches which attempt to preserve as much of the larynx and its function as possible. (b) Hemilaryngectomy (frontal. (a) Epiglottectomy. chondrosarcoma. Vertical partial resection. whereas surgery is considered more effective for larger tumours (T3 and T4) and when there are secondary deposits of carcinoma in the lymph nodes of the neck.

the tumour to be staged and the appropriate operation planned. Specifically for a laryngectomy the patient must be warned that the voice box will be lost and a new technique to speak will need to be learned. A chest radio-graph and liver ultrasound scan are essential (in addition many authorities would advocate a chest CT scan). drains. The patient should be investigated to allow surgery to proceed and to exclude distant metastases. However. The operation should be described and the patient should have knowledge of the wounds. It involves removal of half of the thyroid cartilage. and thyroid and parathyroid supplements may be needed for life following the operation. The patient should be warned before any treatment that there is no guarantee of cure. Excision can be performed using the KTP or CO2 laser. etc. The explanation and warnings should be logged in the case notes. fashioned so as to form a new fixed vocal cord. with an adequate margin of healthy tissue. who should have a relative or close friend present. a permanent end tracheostome will be necessary. Serum urea and electrolytes. nasogastric tube and sutures. Investigations A panendoscopy should always be performed by the surgeon prior to operation. The speech therapist should see the patient preoperatively. It can be performed by an endoscopic or open approach. if on histological . This will allow a representative biopsy to be obtained. part of the supraglottis and the upper half of the cricoid cartilage. Cordectomy This is indicated for a T1-T2 cancer of the glottis which does not reach the anterior commissure or the arytenoid cartilage. Hemilaryngectomy This technique can be used to remove tumours confined to the vocal cord. Consent for total laryngectomy should always be obtained before embarking on any partial resection. liver function tests and a full blood count will be required. The resulting gap is closed by the strap muscles. with the false and true vocal cords. new perspectives will continue to challenge old ones and the current trend is for endocopic laser resection to be offered to patients more often. Patient preparation The patient should have a clear explanation of the diagnosis and what it means. A CT or MRI scan of the larynx should be obtained. Total laryngectomy. It is performed much less frequently in the UK owing to the equally effective results achieved by radiation. It should be remembered that this situation will be distressing for the patient. This procedure therefore has the advantage of allowing some protection for the airway and a reasonable voice for the patient. However. Written confirmation of the histological diagnosis must be in the case notes or the surgeon should have personally spoken to a senior pathologist to confirm the diagnosis of cancer when a frozen section result is presented. Cordectomy also remains a suitable operation for the removal of benign laryngeal tumours.LARYNGECTOMY 145 (b) Vertical subtotal laryngectomy. The patient should be cross-matched for 2 units if a total laryngectomy is proposed. 4.

The first is used for selected glottic carcinomas in which both true and false cords. as a palliative measure in some advanced cases of carcinoma and as a last resort in those who have no voice and chronic aspiration due to palsy of the IXth. Supracricoid partial laryngectomy In the spectrum of procedures available for the surgical management of laryngeal carcinoma. the hyoid and the remaining epiglottis and tongue base. The operation is not suitable if the tumour extends to the base of tongue or vocal cords. and a maximum of one arytenoid cartilage are resected. Emergency laryngectomy An emergency laryngectomy is a laryngectomy performed on a patient with airway compromise due to carcinoma. It should be preceded by direct laryngoscopy to assess the extent of disease and likelihood of successful resection. and joining the lower half of the larynx to the base of the tongue. hence the name crico-hyoid-epiglottopexy. if the patient is over the age of 65 years or if there is intercurrent lung disease. In this case closure is performed by pexy between the cricoid and the hyoid and tongue base. Closure is between the cricoid. The procedure should be avoided by proper planning and if possible by establishing an airway when such patients present. within 24 hours of presentation.146 OTOLARYNGOLOGY examination there has been incomplete resection of the lesion. either postoperative radiotherapy or total laryngectomy should be performed. it is important that the extent of the original lesion is known. Xth and XI th cranial nerves. The aim of these two procedures is excision of tumour and to allow speech and swallowing without a permanent tracheostomy. All patients having a total laryngectomy should have a speech valve inserted at the time of the operation. The technique involves removing the hyoid bone. The procedure that is used for selected supraglottic and transglottic carcinomas results in a more extensive resection. the procedure is called cricohyoidopexy. with removal of the entire epiglottis and pre-epiglottic space. after laryngoscopy and . Supraglottic laryngectomy This is indicated for cancer of the supraglottis (epiglottis and laryngeal vestibule). It is also indicated as salvage surgery in failed radiotherapy. If the operation is to be carried out for post-radiotherapy recurrence. The technique involves removing the entire supraglottis from the vallecula to the ventricle. Cricopharyngeal myotomy is considered an essential manoeuvre to make swallowing easier. the supracricoid partial laryngectomy (SCPL) falls between the vertical partial laryngectomy and the supraglottic laryngectomy at one extreme and total laryngectomy at the other. There are actually two groups of SCPLs. without a prior tracheostomy. the whole thyroid cartilage. therefore. Total laryngectomy Total laryngectomy is indicated for the curative treatment of laryngeal carcinoma when the tumour is considered to be unsuitable for either radiotherapy or a partial resection. thyroid and cricoid cartilages and several rings of the proximal trachea and an ipsilateral thyroid lobectomy or total thyroidectomy. The laser can be used to debulk the tumour and improve the airway. The main disadvantages of this procedure are that the patient’s normal voice is lost and a permanent end tracheostome is required.

Treatment of T3 carcinoma of the larynx by surgery or radiotherapy. Head and Neck Surgeons. Robin PE. This has the advantage of avoiding any surgical disturbance of the regional anatomy. 2000. 17:433–436. 147. This could be due to tumour seeding at the time of tracheostomy. McCombe AW. Lasers in ENT. Second Consensus. Tracheostomy. Jones AS. Tumours of the larynx. Olofsson J. p. 1992. Stridor and stertor. p. Further reading Gibson A. the patient counselled and further treatment planned. In: Scott-Brown’s Otolaryngology. 138. p. 5. Effective Head and Neck Cancer Management. Journal of Laryngology and Otology. Wilson J (ed). London: Butterworths. A number of solutions have been offered to this problem. p. 311. Soler Lluch E. to inadequate resection or to a second primary. 336. Related topics of interest Laryngeal carcinoma. The rationale for emergency laryngectomy is based on the dismal prognosis for any patient who develops a tumour recurrence in their tracheostome: so-called stomal recurrence.LARYNGECTOMY 147 biopsy. Phillips D. Performing a tracheostomy for the relief of airway obstruction due to carcinoma prior to any definitive treatment is associated with a high rate of stomal recurrence. Vol. 6th edn. yet secures the airway while the biopsy results are awaited. The psychological consequences of laryngectomy. Follow-up and aftercare Voice rehabilitation and periodic surveillance for recurrence or second tumour are the main features of follow-up. . 113:349–352. British Association of Otolaryngologists. Clinical Otolaryngology. 1999. 1997. Thyroid function and calcium levels should be checked appropriately. Chaper 11. Some groups have argued that if definitive treatment is undertaken within 48 hours of the tracheostomy the rate of stomal recurrence is not increased. Cook JA.

The wavelength of the photon would depend on the energy difference between the two energy shells and so would be identical for all atoms of a specific element or molecule. Tissue effects The wavelength of light produced. The electron must first be stimulated into the higher energy shell by an external energy source. Technical background All currently available medical laser devices work in a similar fashion. The total power of the beam (watts) is set at the laser control panel. usually electrical. It may then be passed through a lens system for focusing. Through this chamber is pumped the laser medium. another photon will be released. All the effects of lasers are due to the local absorption of energy and the subsequent production of heat in the tissues. and will cause tissue damage which varies with its penetration. partially transmitting mirror at the other. This results in emitted photons. Should this photon strike an atom or molecule identical to that which released the photon and which is in a high-energy state. As this whole process results in the production of heat. collimated (parallel and unidirectional) and coherent (intense and in phase) and therefore represents an extremely powerful. which bounce around the inside of the chamber. high-energy beam. depend on the laser medium used. An optical resonating chamber has a fully reflective mirror at one end and a partially reflective. the optical chamber is surrounded by a water-jacket cooling system. Maiman using synthetic ruby crystals. The . he proposed that electromagnetic radiation (including light) could be produced by an electron of an atom jumping from a high-energy atomic shell to a lower energy shell. This laser burn is extremely accurate. and so its tissue effects. only those parallel to the long axis of the resonating chamber are able to escape through the partially transmitting mirror as laser light. Historical The theoretical foundations for lasers were postulated by Einstein in 1917. Total energy delivery to the tissues is dependent on the power density of the beam and the duration of exposure. the electron which released the photon dropping to a lower energy level. In 1955 microwaves were produced in this fashion and in 1960 the first laser was built by Dr T.LASERS IN ENT Laser is an acronym for light amplification by the stimulated emission of radiation. This light is monochromatic (same colour). thereby releasing a photon of energy. It can be controlled by three methods. travelling in the same direction as that which stimulated the emission. which is stimulated by an electrical current. In essence.

thinner segments of tissue and has more control of the zone of thermal necrosis. It can be used in contact mode with a sculptured quartz or sapphire tip. with a concomitant increase in the power delivered in that time. Types 1. such as the retina of the eye. The holmium:YAG (Ho:YAG) laser. These are becoming increasingly available. the CO2 laser needs to be pulsed (e. It main use has been in laser skin resurfacing. ultrapulse system) or flash scanned (e. 2. 7. This property has made the Ho:YAG laser a candidate for use in sinus surgery which necessitates the removal of bone. but its disadvantage is that its poor penetration will certainly not coagulate blood vessels more than 0. and its effects are extremely localized (0. produces light of wavelength 1064 in the near-infrared range. These are important for the confinement of the thermal energy. The Nd-YAG laser has a crystal of neodymium doped-yttrium aluminium garnet stimulated by a krypton arc lamp. The energy of the CO2 laser is strongly absorbed by any watercontaining tissues. may gradually take over this work. With a wavelength of 2100 nm. The advantage of this is that it can accurately destroy small volumes of tissue with minimal surrounding tissue injury. 4. notably haemoglobin. the KTP being ideal. by being more precise. a bloodless field will only be gained with a more penetrative laser. When excising lesions in tissue with larger vessels. Energy from the argon laser is particularly well absorbed by pigmented tissues. The erbium YAG (Er:YAG) laser. such as the tongue. The Er:YAG has a water absorption coefficient 10 times that of these systems. regardless of pigmentation. Techniques exist for further shortening of the pulse (ultrapulse and Q-switching). 5. Thus it vapourizes narrower. The carbon dioxide laser produces light in the far-infrared range (wavelength 10 600 nm). and so is also invisible. although the KTP laser. this can vapourize bone with little collateral damage. The Nd-YAG is mostly used in fibreoptic bronchoscopy and oesophagoscopy. It is therefore less precise than the other lasers but will coagulate vessels 1. They may be used with optical fibres and have properties similar to those of the Nd-YAG laser with respect to coagulating tissue in non-contact mode and as a ‘hot knife’ in contact mode.5 mm in diameter. Diode lasers. which is advantageous in areas where small haemorrhages will prove disastrous. silktouch system). to produce a beam of 532 nm visible green light.5–2 mm in diameter. Exposure time (seconds) can also be set at the control panel in pulsed mode or left as continuous mode. Consequently it is invisible to the human eye and the system is usually provided with a low-power helium-neon laser carried coaxially to act as a sighting beam. in which a crystal of potassium titanyl phosphate is stimulated by a krypton arc lamp.LASERS IN ENT 149 area of the spot is altered by adjusting the focus of the beam. Tissue penetration is about 1 mm and so it will accurately and reliably coagulate vessels of this diameter.3 mm penetration). For skin surgery in order to achieve correct energy densities. 6. It kills cells by boiling the water content of cells (80% water). which causes a sudden increase in volume and vaporization. Its effect then is that of a hot knife cleaving tissue bloodlessly without deeper effects. The Nd-YAG laser is prone to light scattering and so tissue effects may be evident 2–4 mm from the target site. but mostly 488–514 nm. but those with shorter wavelengths tend to be much less powerful.g. . The argon laser produces visible blue/green light with light at a number of wavelengths.g. To date they are being manufactured to offer wavelengths in the region of 630–1000 nm. 3. The KTP laser is a modification of the Nd-YAG laser. Pulsing reduces the exposure time.

so there is less chance of post-operative airway compromise. Nose. It has also been used to spot weld tympanoplasty grafts in place. It provides at least as good voice preservation after healing. Current research is evaluating the use of lasers for atrophic tympanic membranes and out-patient myringotomies. To protect the endotracheal tube. Anaesthetic. The Ho:YAG has been advocated for use in sinus surgery as it is powerful enough to ablate bone. It should be equipped with remote door-locks to prevent non-essential personnel straying into theatre during laser use. The KTP laser has been used (as a weightless knife) for work around the ossicles. minimizing cochlea trauma. This may change with the evolution of image-guided surgery. Scar tissue formation is also minimized and so the CO2 laser is the method of choice in the excision of benign lesions from the vocal cord. This laser has been used. and on occasion small tumours have . These disadvantages have reduced the popularity of the use of lasers in this instance. 3. It is important to remember that just because a procedure can be done with a laser. Carefully controlled trials are needed to confirm these preliminary findings. argon and Ho:YAG laser have all been described as being of benefit in the management of hereditary telangiectasia.150 OTOLARYNGOLOGY Safety Medical lasers are class 4 and their use requires extreme caution. The CO2. Ear. metal tubes. The argon laser can be used in stapedectomy to divide the crura and fashion a stapedotomy. These include papillomata. The benefit is. The CO2 laser has found most application in ENT in the treatment of laryngeal conditions. the KTP laser will be less likely to cause troublesome bleeding in these instances and will vaporize tissue more efficiently. 2. polyps. It can be used to perform an arytenoidectomy and cordectomy in airway compromise due to vocal cord palsy. Access should be limited to essential personnel only and there should be nominated laser users who are fully conversant with the operation and risks of the laser. nodules and the division of webs. 3. it does not mean that it should be done with a laser. Patient All exposed parts of the patient adjacent to the operating area are covered with damp swabs to prevent any burns. with some success. to perform endoscopic dacrocystorhinostomy under local anaesthetic. It has been suggested that a defocused beam be used to reduce the incidence of residual cholesteatoma in mastoid surgery. Sometimes the laser is not proven to be of greater efficacy than conventional techniques. as well as removing a variety of localized benign intranasal mucosal lesions. Clinical uses A greater range of conditions are now being treated with a variety of lasers. Treatment with this laser results in minimal injury to surrounding tissue and minimal postoperative oedema. which may be vaporized at a high power setting. However. Recent studies have shown that cordectomy for T1 vocal cord squamous cell carcinoma provides a similar prognosis to radiotherapy regarding tumour recurrence. All theatre personnel are required to wear eye protection. tissue splatters and coats the endoscope lens and charring of the tissues obscures the operative field. relatively short lived. however. coated tubes and even jet venturi are used. Personnel. 4. Throat. Environment The operating theatre should be designated a laser area and appropriate warning signs displayed. 1. A number of protective measures are required and include: 1. The CO2 laser has been used to perform linear cautery to the inferior turbinates and turbinectomy. There is a potential explosion risk with volatile anaesthetic agents and oxygen. in the symptomatic treatment of rhinitis. However. Obstructing laryngeal and tracheobronchial tumours may be debulked with this or the KTP laser. 2.

p. Although the CO2 laser may be used for excising lesions of the tongue and oral cavity. Further reading Carruth J. Dilkes MG. . the KTP laser is the method of choice as bleeding is minimal because of its better penetration. Jones N. 1999. 5. Facial skin. ENT News. Laryngectomy. which is stimulated to release singlet oxygen atoms. Steiner W. 138. This technique has found its greatest use in the treatment of skin cancers. These are extremely cytotoxic and result in tumour necrosis. 4. 143. This technique has not found a significant application in ENT although its potential for treating laryngeal cancers and papillomatosis has been investigated. Photodynamic therapy. Cutaneous telangiectasia and port wine stains or flat macular lesions can be reduced by a flashlamp pulsed dye laser and need several treatments. Ultrapulsed CO2 and Er:YAG lasers are used for resurfacing facial scars and wrinkles. 223. 8(4): 10–24. Vocal cord palsy. p. Thick cutaneous haemangiomas do not do well with laser treatment.LASERS IN ENT 151 been completely excised. p. Prescott C. A photosensitive haematoporphyrin derivative which shows preferential uptake by the tumour is administered to the patient. 354. A gold vapour laser emitting a red light is used to activate the photosensitizer. Otosclerosis. A review of lasers in otolaryngology. Robinson JM. p. Related topics of interest Laryngeal carcinoma. Rhinophyma has been treated with the CO2 laser and is cited as causing less intra and post-operative bleeding when compared to scalpel or electrocautery.

Using this should make one focus attention on articles from some journals more than others. many reviewers. perhaps because it is free. Peer review This is the process of reviewers critically evaluating an article that is submitted to a journal for consideration for publication. Journals relevant to otolaryngology ranked by the quality of their peer-reviewer process . unfortunately most of it being poorly directed. even in the highest ranked journals. Table 1. Whilst this objective is highly desirable. Unfortunately. Table 1 is a list of journals most frequently read by otolaryngologists. repeats what is already known. This is mainly because a journal is readily to hand.LITERATURE EVALUATION G. if it attempts to add to knowledge. Or. the research is so poorly designed or executed that the findings are likely to be so grossly biased as to make them invalid. we subscribe to it or it is in the library and we feel it has to be read to keep ‘up-todate’. though it does not remove the need to be critical of articles. the problem is that the majority of what is written. which are informally ranked by the quality of their peer review process. are unable nor have the time to do this properly.Browning Reading the literature is something that most medical post-graduates spend a considerable amount of time doing. often chosen for their prominence in a specialty. The reviewers advise the editor on the scientific merit and suitability of the paper for publication.

we know that there are multiple papers on the topic. to which this one does not appear to add anything. the easier the process becomes. alongside the title of the article. Abstract This will be scanned to ascertain. read no further. In the example in Table 2. if the question posed had been ‘To assess the efficacy…in comparison to the natural history’ or ‘…in comparison to sac surgery’ the reader would move on to their next question. Table 2. which are non-reviewed personal opinions. On the other hand. nor reviews. even though not the readers’ specialty. This task will be made easier if the abstract is ‘structured’ in its format (Table 2) and an objective clearly stated. which are a compilation of papers on the same topic in an attempt to improve the power of the analysis. most of which will not be read further than the title or the abstract. The next question is ‘What is already known about the topic?’ In this case. The more knowledge a reader has on scientific methods and the topic being written about. most would answer ‘Yes’.g. . Example of a structured abstract The reviewers should then ask themselves whether it is a question that would enhance their knowledge or be of practical value to them. most of which are biased selections of the literature rather than ‘structured reviews’ for which there is a formal process (e. Reading a good text book should provide knowledge of what is already known. Reading articles in the top (Table 1) journals. rather than the literature itself where the introduction in papers are often biased reviews of the existing literature. In addition. In this case.LITERATURE EVALUATION 153 This topic takes a systematic approach to evaluating an article. It does not cover editorials. the question being addressed. can increase the former. it does not apply to meta-analyses. Cochrane).

state sensitivity/specificity/ predictive value of diagnostic algorithms versus accepted gold standard. results of a laboratory . Levels of evidence in studies which assess methods of diagnosis of a disease or condition Data which should be presented: Clear definition of characterization of subjects being studied.g. Levels of evidence in studies of management Table 4.g. For continuous outcomes (e. there is a well-established hierarchy of levels of evidence Table 3. For dichotomous outcomes (e.154 OTOLARYNGOLOGY Study designs What is the ideal study design to answer the question posed? For studies that assess the efficacy of management. disease/no disease on X ray).

The most difficult examples of bias to detect are where there is a lack of information. Having identified potential bias. 2. most often unintentional rather than in an attempt to mislead. How similar is the population being studied to the patients the reader deals with? Patients treated in tertiary centres are at the extreme range of the spectrum. .LITERATURE EVALUATION 155 investigation such as audiology). patients can be excluded in a biased manner if they do not fit. (iv) multivariates analysis of risk factor with P-values. What the reader ought to do is to pose the question ‘What if the non-responders had all replied in a particular way. The abstract Table 2 suggests a paper at level III. Papers on diagnostic tests and on aetiology/epidemiology have different criterion (Tables 4 and 5). Response bias. 3. What is being looked for is the highest level available. ‘Receiver-operating characteristics’ (ROC) curve showing test per formance over a range of cut-off values. (v) odds ratios of significant risk factors with 95% confidence intervals. (Table3). In retrospective studies. Look for a description of those excluded. To help detect these a list of things to look for are given. A sample of 100 ENT surgeons produces the following table: The paper should have read ‘between 40 and 89% of otolaryngologists always discuss facial nerve damage with a patient…’. This most often occurs with postal questionnaires where less than 85% of individuals respond. Levels of evidence in studies which investigated the aetiology or epidemiology of a condition Data which should be presented: (i) clear definition of category of subjects being reported. Bias Very few papers are unbiased to some extent. This also can occur in prospective studies. a decision has to be made as to whether it is so gross that the results of the paper are invalid or whether they should be taken with a degree of caution. would the range of outcomes be?’ Using the following example: ‘89% of otolaryngologists always discuss facial nerve damage with a patient prior to mastoid surgery’ based on a 45% response rate. unhappy about the results of treatment). 1. (ii) clear definition of category of controls being reported. (iii) univariate analysis of risk factors with P-values. Table 5. Exclusion bias. One of the reasons why people do not respond could be that they are dissatisfied or at the extreme end of the range of subjects studied (e. (vi) proportion of population to whom risk factors apply with probability of disease occurrence.g. which is the level of evidence for all current papers on this particular topic. Population sample bias. because they need treatment.

Designing questionnaires to assess subjective out-comes is a complicated science and is frequently done incorrectly if at all. Before reading a paper. . to quality of life questions rather than death or an audiogram. but the easiest question to ask is whether a specific questionnaire is appropriate to use in the population being studied. Controls should be identical to the study population in every-thing but the condition being studied. The placebo effect of surgery is large. it must be at least 6–12 months later. 7. the reader should think of the outcomes that they would consider important and then to look to see if the ones chosen satisfy that requirement. Randomization bias. 6. Following is an example of a trial of surgery versus medical management for coronary heart disease with death as the main outcome. ‘Generic’ questionnaires cannot be used in all conditions. This will help exclude papers that describe unimportant outcomes. Non-blinding bias. Analysis bias. whether the bacteria are eradicated or the X ray has improved are irrelevant outcomes. In randomized controlled trials the results should be quoted on an ‘intention to treat’ basis rather than what the patient actually received. Switching between randomization arms is most likely to apply to those allocated to medical management and surgical management. 8. Control bias. Whilst this is of interest. In randomized controlled trials. Bias in choice of outcome. Thus a generic Quality of Life Questionnaire for cancer patients is quite inappropriate to use for hearing-aid patients. knowing that some will change arms during the study?’ (which reflects real life).156 OTOLARYNGOLOGY 4.g. it is not the main question being addressed. Blinding of the individual recording the outcome is usually possible but not of the patient if surgery is being compared with a no surgery aim. Think of what factors affect the outcomes and see if they have been controlled for. Do not be misled by statements such as ‘a validated questionnaire was used’. The temptation here is to compare those actually treated surgically with those treated medically. It is the patient’s symptoms that matter. These factors are called ‘effect modifiers’. 5. those allocating treatment should not in any way be able to decide on what the patient gets. The take-rate of myringoplasty 1 week after surgery is irrelevant. Example of how analysis on an intention to treat basis produces different results from on an ‘abstracted’ basis in a randomized controlled trial. These should be assessed in detail by questions. Here the reader must ask whether the timing of the outcome is an applicable one. Bias in timing of outcome. proven to be relevant in this disease and not covered by a ‘Are you better?’ type question. hence objective outcomes are important when this is being assessed. The means of assessment to ascribe validity are complicated. consider what magnitude the ‘effect modifier’ might have on the results. Thus in papers on chronic rhinosinusitus. Randomisation by an independent party is the ideal method. This particularly applies to subjective rather than objective outcomes. If controls are not identical. e. that is ‘What is the outcome of management strategy A versus strategy B. Blinding is necessary whenever the outcomes can be biased by knowledge of what happened to the patient. 9. nor to decide that once allocated the treatment is inappropriate and exclude the patient.

10. 0=no change. In this particular study it does not matter. Papers that looked at maternal smoking as a single factor would have a positive relationship because smoking is . The latter is the result to take because in real life patients initially allocated to surgery or medical management will switch. Statistical bias. 2=a lot better). P-values should be interpreted with caution. 1=better. look at the number of patients studied. when a statistically insignificant or negative result is being reported. 50 subsequently switched to surgery. The former can be reported as means.LITERATURE EVALUATION 157 % Death rates Of the 373 patients randomized to medical management. Thus. As an example. but this could be due to insufficient numbers of subjects being studied to show this. A P-value of 0. and the question being addressed is what should the initial management strategy be. and taking the statistical rule that if they straddle zero (0) the result is not significant.05 one outcome will be significant as a matter of chance. 26 did not undergo surgery for various practical reasons. 11. there is a lack of power.e. Interpretation bias. when analysed on an ‘as treated’ basis.e. If the 95% confidence interval (CI) of the differences between surgical and medical management are looked at. but in many instances too few a number of subjects is obvious. the results are the same. particularly if it fits in with preconceived ideas.g. there are significantly fewer deaths in the surgical arm. i. from which the percentage mortality on an ‘intention to treat’ basis and an ‘as treated’ basis can be calculated. Type II errors are where no statistical significance was found in a study. but not when analysed on an ‘intention to treat’ basis. The majority of statistical errors are relatively easy to spot. Many papers on aetiological factors fall into the trap of inappropriately linking cause and effect. numerical results with an equal spacing such as height) and ‘nonparametric’ results which may be numerical but not of an equal spacing (e. Of the 394 patients randomized to surgical management.05 means that there is a 5% chance that the association is not statistically significant. Different statistical methods are required for ‘parametric’ (i. let us assume that there is a strong link between lower socio-economic group and otitis media with effusion (OME). The data shows the number of patients that died. with standard deviations and confidence intervals whilst the latter cannot. Take 20 different outcomes and with a P-value of 0. Tables are available which can be consulted to see whether this is the case.

Critical appraisal for clinical problem solving. Butterworth Heinemann. based on a lack of understanding of scientific methodology. British Medical Journal Publishing Group. 2nd edition. 1997. The basics of evidence based medicine. Others can be intentional. On the other hand. et al. Such biases are usually unintentional. there would also be a positive association of having OME with non-ownership of a car. Clinical epidemiology. having read this topic. Sackett DL. Produces an absolute reduction in deaths of 3%. Finally. Each one is valid but gives a different impression of the difference between the two management strategies. How to read a paper. 1997.158 OTOLARYNGOLOGY common in the lower socio-economic groups. et al. Four different methods of describing the difference are shown. Churchill Livingston. Little Brown and Company. 31 people needed to be treated to avoid one death. et al. Such papers could say that this is evidence for mothers to stop smoking to prevent their children getting OME. Munro JF. if a study were to look for it. Evidence-based medicine. The evidence based medicine workbook. Increases survival from 84% to 87%. Such misinterpretations would be less likely if a multifactorial analysis were performed on a full range of factors. Further reading Dixon RA. How to practice and teach EBM. Greenhalgh T. Following is an example of the results of a study where death rates between two management arms are being compared: • • • • Reduces rate of deaths by 20%. 1997. but nobody would suggest giving cars to those that don’t have them to prevent children getting OME. 1991. . A basic science for clinical medicine. based on the data in the third line. Sackett DL. To do this with colleagues in a group or at a course immensely increases their educational value. your critical skills should be honed and regularly used.

to clear granulation tissue from the mastoid air cells and the antrum.Lesser Mastoidectomy is an operation undertaken on the mastoid air cells to remove disease. obviating the need for an obliteration procedure. If cholesteatoma is found. Incisions Either an endaural or postaural incision is used. A myringoplasty is performed at the same time. It provides better access to the sinus tympani and is ideally suited for a small cavity mastoidectomy. Neither will the endaural incision allow an adequate angle of approach to the middle ear in those who perform a posterior tympanotomy (required for combined approach tympanoplasty and to access the round window in cochlear implants). if indicated. It will not allow sufficient posterior access for a subtotal petrosectomy. A properly performed endaural incision will allow good access to the attic. the posterior canal wall may be removed and the procedure converted to a modified radical mastoidectomy. A high-speed drill is used to remove the outer cortex of the mastoid bone and then all air cells. Both are equally popular in the UK.MASTOIDECTOMY T. The disease is usually infective but may occasionally be neoplastic. tegmen and sigmoid sinus even in well-aerated mastoids. Cortical mastoidectomy This is also known as the Schwartze operation and is used for the treatment of the acute noncholesteatomatous mastoiditis when medical treatment has failed or complications have set in.J. The pos-terior canal wall is left intact and the middle-ear contents are not disturbed. Procedure A postaural incision is made at least 1 cm behind the skin fold down to the periosteum. leaving cortical bone over the sigmoid sinus and middle fossa dura. which is elevated to expose the whole of the mastoid. Occasionally a cortical mastoidectomy is performed for severe glue ear. for example endolymphatic sac surgery or insertion of a cochlear implant.H. A cortical mastoidectomy can also be used as treatment for chronic suppurative otitis media when there is no cholesteatoma. including the tip. . It may also be performed as part of a procedure for access to deeper structures. this degree of bone removal is routinely performed by some if there is mastoid disease to allow the postauricular soft tissues to fall into the smooth defect.

. If all the tympanic membrane. The cavity can also be obliterated with bone dust. the attic is removed first. Procedure In a modified radical mastoidectomy the disease is either approached from behind or followed back from the attic. Some cases require an atticotomy only. The graft. It is also useful if an edge of bone is formed for the new tympanic membrane to take off from. is placed under the drum remnant and often over the whole of the mastoid cavity. the zygomatic root. exteriorizing both into a common cavity. Most British surgeons prefer to accept a type III tympanoplasty with the new eardrum in direct contact with the head of the stapes if it is present. and all perilabyrinthine cells. the retrosigmoid. in particular those in Trautman’s triangle. a cortical mastoidectomy is performed and the bridge of the posterior canal wall drilled away to continue removal of the disease from the antrum. the procedure is termed a ‘radical mastoidectomy’. a deep middle ear is helpful and this should be encouraged at the first stage by leaving a lateral annulus. for instance some surgeons try to remove the canal wall in one piece and then replace it at the end of the procedure. This has the advantage that the cavity is only as big as the extent of disease. If a second stage is performed. These procedures will improve the chance of a dry ear and are especially useful in revision surgery. or free muscle. Hearing reconstruction The reconstruction of hearing is dealt with elsewhere. This gives a 5–25 dB conductive loss but profers long-term stability. muscle flaps.g. There are even more variations in the way the reconstruction is done to minimize the chances of chronic or repeated discharge and maximize the hearing.160 OTOLARYNGOLOGY Modified radical mastoidectomy The routine procedure for cholesteatoma is a modified radical mastoidectomy. e. attic and middle ear (atticoantrostomy). The bony work on the cavity itself is of greater importance than the obliteration substance. the cavity edges must be well saucerized. When approached from behind. the middle ear explored and then the antrum opened and the bone removed only as far back as the disease. This may be combined with Eustachian tube obliteration. There are a large number of modifications in the way this operation is performed. If the stapes superstructure is not present. When followed backwards. the hearing reconstruction is best left to a second stage. Many patients opt for no further surgery or a hearing aid if given the choice. The basic reconstruction involves including the Eustachian tube opening in a reconstructed middle ear using a fascial graft. the operation is called a subtotal petrosectomy. Disease-free remnants of the tympanic membrane and ossicular chain are preserved. This type III can be encouraged if the posterior annulus is medialized when lowering the facial ridge so that the head of the stapes is relatively more prominent. usually temporalis fascia. the malleus and incus are removed. closure of the external auditory meatus and filling the cavity with free abdominal fat graft in particularly difficult ears. the mastoid tip removed as far medially as the digastric ridge. This is an operation to remove all middle-ear and mastoid disease. the facial ridge lowered to the level of the inferior canal wall and a wide meatoplasty fashioned. artificial substances. All air cells should be removed. When all the cells of the mastoid are removed. but has to be considered at the same time as the primary surgery even if the tympanoplasty is done as a second stage. the perifacial. hydroxyapatite. This appears to encourage squamous epithelium to cover the cavity and it may allow air from the Eustachian tube to fill deep to it and effectively reform a soft posterior canal wall and a near-normal ear canal. At the second stage a piece of bone or an artificial total ossicular chain prosthesis is placed between drum and footplate.

p. 1986. A cortical mastoidectomy is extended to remove bone posteriorly over the lateral sinus to allow an adequate angle to visualize the middle-ear contents via a posterior tympanotomy in which the posterior part of the middle ear is entered lateral to the mastoid segment of the facial nerve in the angle between it and the chorda tympani. It has a high rate of recurrent cholesteatoma. 38. Tympanoplasty. Great care is necessary when removing disease from the lateral semicircular canal as a fistula can be opened and the resulting loss of perilymph may lead to a dead ear. London: Butterworths. Indeed it may be better to leave disease in situ on such occasions. Related topics of interest Cholesteatoma. 341. the possibility of a dead ear and a chance of postoperative vertigo. Prior to mastoid surgery each patient should be warned about the risk to the VIIth cranial nerve. p. but if performed skillfully it is suitable for patients who are available for long-term follow-up and second. 35. In: Ballantyne JC and Morrison A (eds). The middle-ear part of a mastoidectomy needs equal care to avoid damage to undiseased ossicles.MASTOIDECTOMY 161 Combined approach tympanoplasty This operation removes disease from the mastoid and middle ear. the risk of deterioration in hearing. The facial nerve is always at risk and damage to it is the most obvious disaster that can occur. Complications of mastoidectomy Injury to the anatomical structures of the temporal bone is the main danger for the patient. It is important to document this discussion in the case notes. Rob and Smith’s Operative Surgery. . The combined approach tympanoplasty is the main canal wall up procedure. Chronic suppurative otitis media. This allows access to disease via the ear canal as well as via the mastoid. p. Further reading Ear. The dura and lateral sinus are also at risk. as is the otic capsule.and third-look surgery.

confidentiality is not currently enshrined in statutory law in the UK. even after the patient has died’. In contrast to Continental Europe. However.MEDICOLEGAL ISSUES IN ENT SURGERY M. Public opinion will affect our patients perceptions. It is appalling to contemplate the treatment of patients on the basis of what will be the least likely to land the practitioner in court. It states ‘I will respect the secrets which are confided in me.Roland ‘The regimen I adopt shall be for the benefit of the patients according to my ability and judgement. The main areas covered are: • confidentiality. It is surprising how often this is overlooked in postgraduate courses and texts. there are many complex pressures brought to bear on practitioners to leading them to consider breaching confidentiality. medical ethics or medical litigation. The vast majority of cases of breach of confidentiality occur inadvertently. • consent.F. Rarely a day passes now without the media focusing on some issue of disputed medical practice. • malpractice • negligence • litigation in ENT surgery • complaints against doctors. and not for their hurt or for any wrong. the Declaration of Geneva strongly reinforced the Hippocratic Oath on this issue. it is naïve for any medical practitioner not to have a thorough knowledge of the law and how it is applied.J.’ Hippocratic Oath The aims of the medical practitioner may be laudable. Confidentiality In 1947.Ramadan and N. All healthcare workers should therefore remain constantly vigilant. but all too often when problems occur they become accountable. However. for example overhearing a conversation in a lift or at a reception desk. A patient may enforce confidentiality through a court injunction and an action for damages in a civil . whilst the practice of defensive medicine should be condemned. One day the doctor is hailed as the saviour. The next he is condemned as authoritarian or uncaring. This chapter summarizes the key medicolegal issues and in particular their application to the practice of otolaryngology and head and neck surgery.

he believes that a warning would be harmful to the patients health (therapeutic privilege). The consent form. Consent is implied. should be appropriately qualified and familiar with all the details and risks of the procedure. A surgeon has a duty to explain to the patient in layman’s terms the nature. This provides evidence that consent has been obtained and this should be kept safe in the patient’s record. the patient should be consulted and a new form should be signed. Types of consent.MEDICOLEGAL ISSUES IN ENT SURGERY 163 court may follow any breach. or withhold. but also any staff in their employment. be the one who will do the procedure and. Material risk. if necessary. 3. when a patient undresses voluntarily for examination. a doctor is negligent in failing to mention a risk to a surgical patient was determined in the UK in the case of Sidaway. to supplement verbal explanation using drawings or diagrams to ensure that the patient has sufficient knowledge to make an informed decision. In the Sidaway case. purpose and material risk of the proposed procedure and. consent to examination. Express consent is in an oral or written form. whenever possible. Doctors should answer any question as truthfully and as fully as possible. For major procedures. if not. 4. However. 2. In general practice and private practice the doctor is responsible not only for themselves. The person who obtains the consent should. Oral consent is valid but should be recorded in the case notes. a practitioner can expect to avoid liability if the court finds a reasonable body of opinion which would support the practitioner’s decision. A breach can lead to a charge of serious professional misconduct and erasure from the Register. the court retained the right to over-rule medical opinion if disclosure was obviously necessary for an informed choice by the patient. The legal position on whether. Abbreviation on the consent form should be avoided. Negligence Negligence is established if the duty of care of a doctor towards his patient has been breached (that is when a person has not taken reasonable care to avoid acts or omissions which can cause injury and which can reasonably be foreseen). Under the terms of the Bolam test. for example. It usually falls to the GMC to enforce patient confidentiality on ethical rather than legal grounds. . All staff employed by the NHS may be subject to disciplinary proceedings following a breach of confidentiality. Obtaining consent. Consent may be implied or expressed in the oral or written form. If alteration to the consent is needed. Consent should be countersigned and dated by the same person who gave the explanation. Material risk is that to which a reasonable person in the patient’s position would be likely to attach significance. It may be taken in the out-patients to allow the patient to consider the matter further. which may result in dismissal. In some cases a practitioner may reasonably omit to mention a material risk if. negligence that did not cause damage is not sufficient to bring a medical negligence claim. written consent is usually obtained. or not. investigation or treatment. This right is founded on the moral principle of respect for autonomy. but this needs to be checked again on admission in case there has been a change in the patient’s condition. after proper consideration of the patients condition. The patient must have sufficient time to think of the procedure and should not be taken under any form of duress. or take advice. Consent is obtained before the procedure and before sedation. 1. Consent The competent adult patient has a fundamental right to give.

One should always believe the patient. but when they actually understand what it looks like. This was perceived by him as insignificant. lack of clarity. standards will change with the passage of time (more progress and knowledge). The Bolam test now applies extensively in all areas of medicine. Failure of communication among the hospital staff can also be a source of complaint. Frien HMC. 1957). unrealistic expectations. including diagnosis. Patients’ letters. because the patient had thought that it was 2% loss of his ability to hear clearly not 2% risk of absolute deafness). Complaints against doctors Complaints against doctors are rising and the main cause for this is lack of or inadequate communication with the patients. Duty of care can be discharged if the patient is referred to or advice taken from a senior colleague. treatment and information disclosed to patients to obtain a true consent. A clear and honest explanation to the patient often avoids or aborts an imminent complaint. not necessarily the majority. the judge directed the jury that a doctor is not guilty of negligence if he has acted in accordance with a practice accepted as proper by a responsible body of medical men skilled in that particular art. For most patients. the case of the patient who was told that there is a 2% risk to the hearing. Therefore. again. Your communication with the patient should also be expressed clearly in the records. Doctors need to communicate better. avoiding medical jargon. but a doctor is expected to display the skill and care of a reasonably competent colleague. to listen to the patient and to speak to the patient in a language which can be understood. it is acceptable to provide different treatment from a colleague as long as it is accepted by a reasonable body of medical opinion skilled in that specialty. What to do when things go wrong . medical terms and one needs to speak to the patient clearly when diagnosis and treatment are explained and risks and realistic expectation of treatment are quoted. The majority of patients seem to react reasonably to warnings of facial paralysis. such as when one hands over care of patients when going on holiday. and indeed often do not understand. The art of good communication also covers the areas of patients calls to you or your secretary. lack of communication was evident. Naturally. but when he had a ‘dead’ ear after the operation. if possible.164 OTOLARYNGOLOGY The standard of care provided is not an absolute. Patients do not like to be rushed out of the clinic. It will do no harm to improve the line of communication by checking with the patient in plain words whether he or she has understood all that has been said. highlights how important it is that obtaining consent for surgery requires a great deal of clarity. the patient must know what facial paralysis means and looks like and one must quantify for the patient the percentage of risk and success. The patient suffered injuries and fractures but because some doctors do avoid muscle relaxants because of their side effects. For example. ECT treatment was given to a patient without a muscle relaxant. This. In the Bolam case (Bolam vs. whether he or she would like to ask further questions and to ask the patient to get in touch if there is a problem with follow-up arrangements. all that is required is an explanation of what happened and why things went wrong. Patients do not like. reaction is different. patients’ suggestions for further investigation or different treatment by correspondence should be respected. Many complaints arise as a result of poor communication (informed consent. Patients like to know that he or she is the most important person in your life during the consultation and always want to feel that their personal agenda has been expressed fully during the consultation. Different doctors genuinely vary in their management of an illness. For example.

Outpatients Procedures. Make sure that all swabs are correct after surgery and that bandages are not too tight. Write clearly in the case notes what happened and what has been said. because of the pride and faith doctors have in their own profession. Unclear medical notes will not help the case against you. Failure or delayed diagnosis is particularly risky in certain areas. Do not file your copy to the Legal Adviser in the case notes. such as malignancy. But remember not to let self-doubt creep in. Figures from general practice show that almost 20% of all claims arise from ear syringing (a procedure often delegated to a practice nurse). The most common reason for a completed ENT claim involves some sort of dental damage during an ENT procedure. 2. Educate yourself further in the subject. not only of the medication but of the options without the medication. Potential harmful effects of prescribed medication should be clearly explained and documented. Similarly. In a busy out-patient department. Areas where special precautions should be taken are diathermy and laser (burn) and damage to the teeth during endoscopy.MEDICOLEGAL ISSUES IN ENT SURGERY 165 • • • • • • • • Explain clearly and honestly what happened. informed consent can be forgotten and this causes complaint. sight.e. smell or taste. For example there has recently been successful litigation in this area by patients receiving ototoxic ear drops. it is naturally very upsetting when a complaint is made against a doctor who treated their patient with the best intent. Medical records which are tampered with or missing may turn a defensible case into an indefensible one. for things have the habit of not turning out to be as bad as they first appear. The common reasons for this are poor technique. It is necessary that the patient understands what facial palsy is. A written account of what is said. excess pressure and failure to examine the ear. for often that is all the patient or their relatives need. They provide invaluable evidence of treatment given in the event of a claim. Finally. . It can be difficult in others. investigations and pre-operative photography should be documented. Litigation for delay or failure to diagnose is on the increase. It is not sufficient to warn the patient who is to undergo mastoid surgery of facial palsy. Useful advice on this is given by the BAO-HNS. 1. give a follow-up appointment. i. Patients unsatisfied for being hurried out of the consulting room may feel the cause for a complaint. Never tamper with the patients records. Patients receiving systemic ototoxic medication ought to be assessed audiometrically and the risks explained to the patient. Always date clearly any addition to the notes. the pros and potential problems of oral/topical steroids should always be explained. faulty equipment. such as untypical presentation of acoustic neuroma. continue to keep a good relationship with the patient. Avoid being defensive. diminished hearing. Areas of litigation in ENT Medical Defence Union figures show that the most common reason for the notification of an ENT claim relates to some form of sensory loss following surgery. keep your Legal Advisor informed and keep faith. In-patient procedures Good communication in layman’s terms continues to play a major role so that the patient forms realistic expectations. Complete and contemporaneous medical records are essential. keep good records. contact the Legal Adviser or Medical Defence Union immediately. If appropriate.

GMC Publications. legal and political issues that affect the way in which we work. Bolam -v. occupation and type of disease have to be taken into account when taking consent. Journal of MDU. Butterworth. one should remember that courtesy. 13. ethical.166 OTOLARYNGOLOGY Each patient is a different individual. Vol. No. His or her circumstances. 1996 revised November 1997. 1 February 1997. 1957. 1991. age. Hospital Management Committee. competence and communication are the cornerstone of good medical practice (the three Cs). MDU Ltd. Conclusion Although there are exhaustive lists of moral. Further reading Handbook of Medicolegal Practice.Frien. MDU Consent to Treatment.. Seeking Patients Consent—the Ethical Consideration. . General Medical Council.

Patients are usually seen in the clinic between attacks. Bilateral disease is thought to occur in about one-third of cases. Patients are typically in their fifth decade at presentation with no gender bias. Episodic vertigo and hearing loss are the main complaints. of a condition characterized of episodic vertigo. Clinical features Menière’s disease accounts for between 10–20% of cases of true vertigo in a typical outpatient population. There is no doubt that a large psychological component exists. although hearing in the affected ear invariably tends to deteriorate. . The same pressure increase leads to distortion of the ampullae of the semicircular canals with subsequent vestibular dysfunction. Regardless of the primary cause. there follows expansion of the endolymphatic compartment. The increased endolymphatic pressure leads to an alteration in basilar membrane mobility. endolymphatic hydrops. resulting in hearing loss and tinnitus. In the early stages of the disease the hearing may return to normal after the attacks. Movement may exacerbate the vertigo so the patient will lie as still as possible during an attack. Attacks vary in frequency but typically last between 1 and 24 hours and are often associated with systemic upset in the form of nausea and vomiting. Current theories of aetiology include labyrinthine ischaemia and an autoimmune response following a viral infection. leading to the delicate neural tissues being exposed to potassium-rich and neurotoxic perilymph with further provocation of symptoms. The condition is punctuated by frequent remissions and relapses over a time period of many years. which is thought to give rise to the classical symptoms. the aetiology of this condition still remains unknown. Pathophysiology Despite mountains of research. but if the condition progresses and attacks recur deafness becomes established and more severe. and consequently physical examination is normal. although tinnitus and a sense of fullness in the affected ear are not infrequent. In the long term (10 years) over 75% of patients’ vertiginous symptoms will improve regardless of treatment type. tinnitus and deafness. in 1861.MENIÈRE’S DISEASE Menière’s disease has been recognized since the first description by Prosper Menière. Nystagmus is present but its direction is not indicative of the side of origin of the symptoms. In severe cases rupture of Reissner’s membrane may occur.

e. Although 90% of patients report initial satisfactory symptom control. although the morbidity is higher as a neurosurgical approach is required.i. Medical treatment should provide adequate symptom control in about 80% of patients. acoustic neuroma). The vestibular labyrinth may be selectively destroyed by the use of ultrasound. by 5 years this figure is down to 60%.g. maintained for up to 10 years. particularly hearing. Betahistine 16 mg t. This procedure is without any logical or scientific support and probably works by placebo effect alone. Medical. with an appropriate history. are frequently prescribed but there is no good study to demonstrate any greater efficacy than placebo in this condition. have been reported. 2. Other causes of intermittent vertigo should also be excluded. climbing from the simple to the complicated. Treatment can be either medical or surgical and can be regarded as a therapeutic ladder. it can be used as a preoperative assessment of the potential response to conservative surgery.. thiazides in particular.d. such as prochlorperazine and cinnarizine. in which sac surgery was prospectively and randomly compared with simple cortical mastoidectomy. but this technique does also risk cochlear damage. Decompression is achieved by exposing and opening the sac with or without the use of a shunt to provide prolonged drainage. Electrocochleography may show an enhanced negative summating potential indicative of altered cochlear function. Classically this loss is described as low frequency. Diuretics. are without doubt useful in short-term symptom control and are best prescribed to be taken at the onset of any attack. is good evidence for the diagnosis. The mainstay of surgery for this condition has been decompression of the endolymphatic sac with the aim of treating the underlying pathophysiological abnormality without destroying the function of the ear. This is accomplished via a cortical mastoidectomy approach to the sac as it lies in the posterior cranial fossa. Control rates of 90%. Surgical. but in fact is flat in two-thirds of cases. 1. Medical treatment starts with the manipulation of diet in an effort to reduce salt and fluid intake. In those patients with an asymmetrical hearing loss. and strong psychological reassurance. which abolishes signals from the troublesome labyrinth while still preserving hearing. regardless of which treatment modality is ultimately used (i. A fluctuating sensorineural loss shown on consecutive audiograms over a period of time. The triad of symptoms of episodic vertigo. It can also be achieved by the local application of gentamicin at the round . The study was blind and demonstrated no significant differences between the two surgical options. Vestibular sedatives. tinnitus and deafness is sometimes described as Menière’s syndrome. The glycerol dehydration test works on the principle that dehydrating the cochlea and thus reducing the endolymphatic hydrops will produce an improvement in the audiogram and the ECochG. There are causes of this other than Menière’s disease.168 OTOLARYNGOLOGY Investigations An audiogram is essential and may show evidence of a sensorineural hearing loss. strong placebo effect). More radical surgery for this condition involves vestibular nerve section. The simplest surgical procedure is the insertion of a grommet in the affected ear. a labyrinthine vasodilator. has been shown to give significantly greater symptom control than placebo. Management It is important to bear in mind that Menière’s disease is a condition that responds well to a supportive and sympathetic therapeutic approach. The greatest controversy surrounding endolymphatic sac surgery concerns the Danish sham study in 1981. it is essential to exclude a cerebellopontine angle tumour (e. but is unpleasant for the patient as it causes nausea and headache. and caloric tests may demonstrate impaired vestibular function.

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window, or by insufflation of gentamicin using an indwelling middle ear catheter. Finally, in those ears with poor hearing a surgical labyrinthectomy may be the procedure of choice. Follow-up and aftercare By the very nature of the condition, these patients are often ‘long-term’ attenders at an ENT department. However, with appropriate support and encouragement, they need not be ‘frequent’ attenders. Further reading
Ludman H. Menière’s disease. British Medical Journal, 1990; 301:1232–1233. Ruckenstein MJ, Rutka JA, Hawke M. The treatment of Menière’s disease: Torok revisited. Laryngoscope, 1991; 101: 211–218. Commins DJ and Nedzelski JM. Topical drugs in the treatment of Menière’s disease. Current Opinion in Otolaryngology and Head and Neck Surgery, 1996; 4:319–324.

Related topics of interest Caloric tests, p. 27; Vertigo, p. 346; Evoked response audiometry, p. 78; Vestibular function tests, p. 350.

NASAL GRANULOMATA

A granulomatous reaction is a specific type of chronic inflammation characterized by the local accumulation of macrophages and their morphologically and functionally diverse derivatives. These comprise the epithelioid cell and multinucleate giant cell. Usually surrounding and interacting with these is a zone of lymphocytes. Most nasal granulomata are formed as a result of specific chronic infections. The most important of these are tuberculosis, syphilis, leprosy and fungal infections. Non-specific granulomata occur when no infectious agent can be defined and comprises sarcoidosis and Wegener’s granulomatosis (WG). The formerly and inappropriately named lethal midline granuloma is now recognized to be a high grade T-cell lymphoma. Wegener’s granulomatosis Wegener in 1939 described a granulomatous disease of unknown aetiology comprising destructive lesions of the upper and lower respiratory tracts and glomerulonephritis. Histological examination showed granuloma formation and necrotizing vasculitis. It is now accepted that only a single system may be affected by the disease or there may be multi system involvement, affecting not only the three classical systems but also virtually every organ in the body including the ear. These are considered to be variations of WG, but no consensus view exists on the nomenclature in these situations. Pathogenesis Current knowledge suggests that an infection, usually viral, in susceptible individuals triggers an immunological response to produce the features of WG. Clinical features In the nose and when active WG classically causes a sanguinous discharge, crust formation and friable ulcerated mucosa. Chest features comprise haemoptysis and dyspnoea. Oliguria and micro or macroscopic haematuria suggests renal involvement. The patient feels weak and lethargic and experiences marked weight loss. Untreated there is a 93% two-year mortality. WG may effect the external and middle ear causing a serosanguinous discharge and a conductive hearing loss. Vestibulocochlear symptoms, a facial palsy and a secondary infection may occur. On examination the appearances are similar to a carcinoma and the diagnosis can only be made by a representative biopsy. Friable, ulcerative lesions in the mouth, oropharynx, and larynx have also been described.

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Investigations A chest radiograph may show single or multiple opacities up to 5 cm in diameter compatible with areas of infarction with or without cavitation. Alveolar infiltrates, pleural opacities or atelectasis may be present. Urinalysis may show red cells, protein and casts. Creatinine clearance declines. Renal biopsy, if indicated, shows focal necrotizing glomerulonephritis and vasculitis. A recent meta-analysis of patients with active WG calculated a sensitivity of 91% and a specificity of 99% for cytoplasmic anti-neutrophil cytoplasmic antibody (c-ANCA). Between 20 and 40% have raised titres against p (perinuclear)-ANCA. Both antibodies are detected by indirect immunofluorescence. Both antibodies are directed against proteinase 3 and therefore low titre samples can be checked by an antigen-specific enzyme-linked immunosorbent assay. These titres parallel changes in disease activity. The classical three system involvement and a representative biopsy of an active area is both necessary and sufficient to make the diagnosis. Random biopsies of normal looking upper respiratory mucosa in subjects suspected of having the disease provide a zero WG diagnostic yield and therefore the biopsy of an active area is stressed. Treatment Long-term, low-dose antibiotic therapy aimed at preventing an infectious trigger or immunosuppressive therapy aimed at dampening the immunological response is the current strategy. Low-dose co-trimoxazole has been shown to prevent relapse in many patients. Septrin has been shown to increase host cytotoxicity and enhance intracellular killing. Cell mediated immunity against viruses involves the intracellular killing of free virus particles and the killing of virus infected cells by macrophages. Co-trimoxazole’s mechanism of action may be to enhance virus killing sufficiently to prevent immune complex formation which causes inflammation and granuloma formation when deposited in the micro circulation (see Related topic). Cyclophosphamide and prednisolone are the current immunosuppressive drugs of choice, the doses of which are adjusted to reduce side effects to a minimum while maintaining remission. In patients with resistant or fulminant disease plasma exchange, high-dose intravenous steroids or extracorporeal immunoabsorption with protein. Disease activity can be monitored by the ESR and serum C-reactive protein level. High grade T-cell lymphoma This was often confused with WG, but with the advent of modern immunocytochemical techniques, a representative biopsy will allow an accurate diagnosis. Clinical features The nasal features are similar to WG but there is little systemic disturbance and in particular no bronchial or renal disease. There is progressive destruction of the mid-facial structures. Untreated the patient succumbs from secondary infection or cachexia. Investigations A representative biopsy will show huge numbers of small cells with a high incidence of mitoses. There may be zones of acute inflammatory cells if a secondary infection supervenes. Necrotizing vasculitis and granuloma formation are absent. As the small cells may represent a poorly differentiated squamous cell

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carcinoma, malignant melanoma, neuroblastoma or rhabdomyosarcoma immunocytochemical analysis is necessary to confirm the diagnosis. Staging should be undertaken by a medical oncologist to determine optimum treatment. Treatment 1. Antibiotics to control secondary infection. 2. Surgical debridement of necrotic tissue. 3. A curative dose of radiotherapy, usually 60–66 Gy in 30 fractions if stage I (localized) disease, followed by further debridement if indicated. 4. Reconstructive surgery to the nose and mid facial regions as required. Syphilis and tuberculosis Only tertiary syphilis produces a granulomatous reaction, the pathological lesion being the gumma. This can invade mucous membrane, cartilage or bone, the bony septum being the site most commonly involved. The usual presentation is nasal swelling, putrid discharge, bleeding and crusting. A red nodular swelling which can be diffuse or localized may be visible. The treponema pallidum haemagglutination test (TPHA) and fluorescent treponemal antibody test (FTA) for syphilis are positive and a biopsy of the lesion shows perivascular cuffing of arterioles by chronic inflammatory cells and endarteritis. There maybe a septal perforation, erosion of the nasal bridge with a saddle deformity, stenosis of the nares or atrophic rhinitis. Tuberculosis and sarcoid affect mainly the cartilaginous septum. In tuberculosis there may be apple jelly nodules around the vestibular skin and signs of pulmonary involvement. Biopsy shows caseating granulomata and acid fast bacilli may show on a Ziehl-Neelsen stain or following culture. Biopsy of a sarcoid lesion shows non-caseating granulomata, angiotensin converting enzyme levels are raised, the Kveim test is positive and there may be evidence of multi-system involvement. Scleroma and rhinosporidiosis Scleroma is a disease affecting any area of the upper and lower aerodigestive tract and caused by a gramnegative diplococcus Klebsiella rhinoscleromatis. It is endemic in India, the Middle East and parts of Africa but unusual in Western countries when it usually arises within the immigrant population. Nasal symptoms are the most common and usually comprise nasal obstruction and foul smelling mucopurulent rhinorrhoea. Signs of a severe bacterial rhinosinusitis with mucosal injection and oedema, and mucopurulent discharge may be present on endoscopic examination. There may be submucosal swelling in the vestibular area. Atrophic rhinitis like crusting and septal perforation may occur in the cicatricial phase. The diagnosis is made by culture of the diplococcus. Mikulicz cells (macrophage with clear cytoplasm containing the encapsulated organism) and Russell bodies (bright-red degenerated plasma cells) are classically seen on histology. Ciprofloxacin or co-trimoxazole are the antibiotics of choice and need to be continued for at least a month as the organism is difficult to kill because of its mucopolysaccaride coat. Rhinosporidiosis is a chronic disease which can affect any skin lined or mucosal surface of the body and occasionally the viscera. It is caused by Rhinosporidium seeberi and it is thought to be a fungus rather than a protozoan. It is transmitted by swimming in infected water. It is most commonly found in India and Sri Lanka. The nose is the mostly commonly infected site and the disease is typically insidious in onset and runs a slow course. In the early stages a thick, sticky nasal discharge may be seen and there is usually a

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history of recurrent epistaxis. Thereafter pedunculated or sessile, soft, injected polyps form typically around the nasal vestibule. The organism has not been cultivated in vitro or transmitted to animals in the laboratory. Chemotherapy is universally unsuccessful and the only treatment is surgery to excise the lesions. Further reading
Van der Woude FJ, Van Es LA, Daha MR. The role of the c-ANCA antigen in the pathogenesis of Wegener’s granulomatosis. A hypothesis based on both humoral and cellular mechanisms. Netherlands Journal of Medicine, 1990; 36:169–171. Rao JK, Weinberger M, Oddone EZ, Allen NB et al. The role of antineutrophil cytoplasmic antibody (c-ANCA) testing in the diagnosis of Wegener’s granulomatosis. Annals of Internal Medicine, 1995; 123: 925–932. Marfatia HK, Kirtan MV. Management of rhinosporidiosis—newer concept. Indian Journal of Otolaryngology Head and Neck Surgery, 1997; 49:73–74.

Related topic of interest Sinonasal tumours, p. 280; Sinusitis, p. 285.

NASAL POLYPS

Aetiology In certain predisposed individuals, any inflammatory nasal condition can lead to marked swelling of the sinus and nasal mucosa. This seems particularly to affect the mucosa in the region of the middle turbinate and middle meatus. When this swelling becomes sufficiently pronounced, polyp formation may result. The initiator of this inflammatory response may be chronic infection, allergy or intrinsic rhinitis, but in some cases the cause is unknown. Recent work suggests that patients who develop nasal polyps have a subtle immunological disorder of the upper (and often lower) airway; co-existent asthma is common. Pathology Pathologically, polyps demonstrate marked oedema of the connective tissue stroma, which also contains a variety of inflammatory mediators such as histamine, prostaglandins and leukotrienes. There is a marked eosinophilic and histiocytic infiltrate and the epithelium displays goblet cell hyperplasia and in some areas a squamous cell metaplasia. A polyp forms when the oedematous stroma ruptures and herniates through the basement membrane. Nasal polyps are rare in childhood, and if they occur one should suspect cystic fibrosis or immune deficiency. Recurrence is common after surgical removal, although it may often be delayed for many years. It is more likely and tends to occur sooner in those patients with coexistent asthma and aspirin hypersensitivity. Clinical features Nasal polyps may be asymptomatic, but even when small most patients complain of a feeling of congestion or obstruction high in the nose and a hyponasal quality to their speech. As the polyps enlarge there is associated worsening of nasal obstruction and usually a profuse watery nasal discharge causing rhinorrhoea or a postnasal space drip. At the same time patients frequently complain of loss of taste and smell. Headaches, pressure sensation in the face and sinusitis may occur. In severe cases the polyps may be visible at the external nares and widening of the intercanthal distance may occur. The polyps are insensitive. A history of epistaxis or contact bleeding should raise suspicion of the possibility of a neoplastic polyp. Clinical examination of the nose is not complete without an endoscopic examination (rigid or flexible), as without it small polyps in the middle meatus may be missed.

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Investigations There are few essential investigations. It is worth performing skin tests or a PRIST and RAST to identify an allergic cause. Sinus radiographs may be helpful in demonstrating maxillary sinus involvement but are rarely used. In recurrent cases and those to be treated by FESS, coronal CT scanning of the sinuses is essential and provides far more anatomical and diagnostic information. Following surgical removal the polyps should always be sent for histological analysis, especially unilateral polyps or unusual-looking polyps. Management 1. Medical. In patients with small polyps and following surgical removal it is worth trying medical therapy. This consists of intranasal steroids, as either drops or spray, with the addition of oral antihistamines if there is an allergic element. Short courses of low-dose oral steroids may be extremely useful in those patients with particularly aggressive polyposis. 2. Surgical. If sufficiently troublesome surgical clearance can provide marked symptomatic improvement. Good symptom control can be obtained with a ‘simple’ intranasal polypectomy under either local or general anaesthetic. It is likely that a more thorough clearance can lead to better longer-term disease control and so an ethmoidectomy may also be performed. The majority of surgeons would now probably undertake this procedure endoscopically. With appropriate preparation of the operative field and the excellent vision afforded by the endoscope, an exceptionally thorough clearance can be undertaken. This is now often augmented with the aid of powered suction and microdebriders. Computer-aided navigation systems for ethmoid sinus surgery are available and may increase safety in difficult regions, such as the frontal recess. Follow-up and aftercare In simple cases no long-term follow-up is required after the first post-operative check; the patient can be asked to return should future problems arise. Intranasal steroids have been shown to reduce recurrence in the first year and may make a difference to the recurrence rate given long term. In severe cases oral steroids may be needed following surgery. Periodic surveillance and follow-up are usually required. Antrochoanal polyp The antrochoanal polyp is uncommon. It is typically unilateral and commences as oedematous lining from the maxillary sinus. This lining prolapses through the ostium into the nasal cavity and enlarges towards the posterior choana and nasopharynx. The patient, commonly a young adult, complains of unilateral nasal obstruction, which is worse on expiration owing to the ball valve-like effect of the polyp in the posterior choana. If sufficiently large, it may produce bilateral obstruction and cause otological symptoms as a result of blockage of the Eustachian tube orifice. Anterior rhinoscopy may look normal as only the thin stalk may present in the nose. The enlarged posterior end may be seen on posterior rhinoscopy. All suspected cases should therefore have proper endoscopic examination. A CT scan is the best investigation, but a plain sinus radiograph of the maxillary sinus may show complete opacification of the affected antrum.

Sinusitis. p. An intranasal antrostomy is the usual approach. p. This can usually be achieved endoscopically. p.176 OTOLARYNGOLOGY Treatment is by complete nasal avulsion with removal of the antral portion. Functional endoscopic sinus surgery. 285. Related topics of interest Allergic rhinitis. Intrinsic rhinitis. . Failure to remove the antral lining may result in a recurrence. 11. and Mackay IS. Current Opinion in Otolarygology and Head and Neck Surgery. p. Management of nasal polyps. 131. Further reading Rowe-Jones JM. With recurrence a Caldwell-Luc procedure may be required to clear the sinus. 6:41–46. 108. 1998.

note any deformity and exclude a septal haematoma. It is appropriate in uncomplicated cases to reassess the patient 5–7 days after the injury. Check the nasal airways and examine the septum. Injury to the nose may result in a combination of soft-tissue injury. A history of trauma to the midface accompanied by epistaxis. The perpendicular plate of the ethmoid rotates backwards and the septum collapses into the face. Clinical features Trauma to the nose may be part of a more extensive injury to the facial skeleton and base of skull. CSF leak and facial bone fracture. a noticeable deformity and nasal airway obstruction are the usual complaints. A class 2 fracture is nearly always due to lateral trauma and results in a horizontal (Jarjavay fracture) or C-shaped fracture of the septum involving the perpendicular plate of the ethmoid and the septal cartilage in combination with a fracture of the frontal process of the maxillae. If the nose is fractured by high-velocity trauma then facial fractures are often an accompaniment. There is a marked depression of the nasal bones. A class 3 fracture indicates that the velocity of the trauma has been even greater and results in a nasal fracture which extends to include the ethmoid labyrinth. haematoma and swelling may make the assessment difficult. and there is an apparent widening of the space between the eyes (telecanthus). previous episodes of trauma and whether the nasal deformity is new or old. fracture of the nasal bones. septal haematoma.NASAL TRAUMA The commonest causes of nasal trauma are assault. Classification of fracture of the nasal bones An isolated nasal fracture is usually caused by low-velocity trauma. The nasal swelling is often accompanied by periorbital and subconjunctival ecchymosis. Nasofrontoethmoid fractures may produce symptoms of diplopia and epiphora. Remember to enquire about any trauma to the head and neck and any other injuries. It should be remembered that the most important consideration in maxillofacial injuries is the maintenance of an airway. Ocular movements should be tested and Vth . Nasal fractures are classified on a 1–3 scale depending on their severity and extent. Nasal trauma does not imply only nasal fracture. road traffic accident and sports injuries. A class 1 fracture is usually due to a frontal or fronto-lateral blow and results in a vertical fracture of the septum (Chevallet fracture) with a depressed or displaced distal portion of the nasal bone. It is important to carefully record the time and nature of the trauma. fracture or dislocation of the septum. turning up the tip of the nose and revealing the nostrils. which are pushed under the frontal bones. Tenderness.

face and nasal bones depending on the extent and severity of the injury. There is usually complete bilateral nasal obstruction caused by a soft swelling.178 OTOLARYNGOLOGY nerve function (infraorbital sensation) and dental occlusion should be checked. which will approach that of serum levels. 3. Manipulation should never be delayed for more than 2 weeks post injury because the nasal bones will fix and reduction will be difficult if not impossible. Small lacerations can be closed with Steristrips. but incision and drainage with quilt suturing (to obliterate the dead space) is required if the collection reaccumulates. but in more serious injuries radiographs are an important investigation. If this is missed or not treated correctly. one blade in the nasal cavity and the other outside. They may be important for medicolegal purposes. or alternatively 2-transferrin assays (this is a protein present in perilymph and CSF) can be used. The elucidation and documentation of these clinical symptoms and signs should be standard medical practice. 2. Appropriate antibiotic and antitetanus cover should be given. It is possible to reduce a simple class 1 fracture under local anaesthetic before any swelling appears if it is seen early enough. Class 2 fractures have a propensity to redisplace owing to overlapping of the fractured ends of the septal cartilage and the perpendicular plate of the ethmoid. Wounds are thoroughly cleaned and any foreign body removed. 4. If the fracture is seen later and there is much swelling. Treatment is not required in some patients because there is no fracture or bony deformity. Disimpaction and realignment can usually be achieved with laterally applied digital pressure and Walsham’s forceps. Soft-tissue injury. Cerebrospinal fluid leaks. The patient should be given a course of antibiotics to reduce the risk of local and systemic infection.g. They should include views of the skull. Malunion following nasal trauma will require treatment by a formal septorhinoplasty procedure. cartilage necrosis and nasal saddle deformity may ensue. Confirmation of the diagnosis is obtained by checking the glucose content of the rhinorrhoea. Septal haematoma. They are also important for medicolegal purposes. Nasal fracture. The septum is approached through a Killian incision with the aim of pulling the rotated septal cartilage forwards and downwards. Abrasions are best left open. The depressed nasal bones need to be elevated out of the face and supported with wires via an incision over the nasofrontal angle. A CT scan on bone setting may delineate maxillofacial fractures when there is uncertainty. rarely. All injuries should be carefully documented in the case notes supplemented with drawings and occasionally photographs. manipulation should be delayed for 5–7 days. It is also inappropriate to try and manipulate a long-standing deformity as this will inevitably result in failure. The manipulation of the nasal bone should be accompanied by an excision of the septal fracture and overlapping segments through a Killian incision. Management 1. Investigations In the majority of simple uncomplicated fractures no investigations are required. submucosal resection (SMR)) and. These patients should be reassured and reviewed again when swelling has subsided. Aspiration may suffice if the haematoma is small. blood dyscrasias. The cribriform plate is extremely thin and is the commonest area of fracture. but it can also occur as a complication of septal surgery (e. It may follow nasal trauma. This is due to a collection of blood beneath the mucoperichondrium of the nasal septum. The presence of clear rhinorrhoea at any stage following nasal trauma should raise the suspicion of a CSF leak. a septal abscess. A class 3 fracture will require an open reduction. but larger lacerations should be closed with fine monofilament sutures. Fluorescein injected into the CSF via a lumbar puncture can be collected .

Vol. 1997. Until the leak ceases the patient is at risk of pneumococcal meningitis and most advocate oral penicillin and sulphadimidine as antibiotic prophylaxis. 278. Many leaks will close spontaneously. Septal perforation. Current Opinion in Otolaryngology and Head and Neck Surgery.NASAL TRAUMA 179 from the leak in the nose. High-resolution CT scan may delineate the fracture. In: Mackay IS. Scott-Brown’s Otolaryngology. 4. Repair can be approached by an external ethmoidectomy. a trans-septal route. by an intranasal endoscopic approach or by a frontal craniotomy and repair with reduction of the bony fragments. 84. Some suggest that antibiotic prophylaxis is not required. 1994. 6th edn. but some will require surgical repair with temporalis fascia. p. fascia lata or a mucosal flap from the nasal septum. Further reading Gleeson M. Related topics of interest Examination of the nose. Bull TR (eds). London: Butterworth. Nasal and sinus trauma. 1–36. Vuilleriun T. . Fractures of the facial skeleton. Imola M. 2:37–41. p.

• WHO type 2b is undifferentiated carcinoma. the male population of which comprise the world’s highest at risk population group. The environmental factor most widely implicated is salted preserved fish. • WHO type 2a is nonkeratinizing squamous cell carcinoma. NPC cells consistently express two species of EBV proteins. The latter has a predilection for those of Southern Chinese or Hong Kong extraction forming 20% of all malignancies in these people and 80% of their head and neck cancers. . EB nuclear antigen 1 and latent membrane protein 1 detectable by immunofluorescence. • WHO type 1 is keratinizing squamous cell carcinoma. Angiofibroma. Nasopharyngeal carcinoma Pathology NPC can be divided into three subtypes based on the World Health Organization (WHO) classification. Aetiology The consensus view supports the proposal that in the genetically predisposed a carcinogen is triggered by an environmental co-factor to transform nasopharyngeal epithelial cells. a staple diet of the Hong Kong boat people. In particular: 1. 2. It divides the cancer on the basis of its light microscopy appearance. Southern Blot and Polymerase Chain Reaction consistently detect DNA sequences of EBV in NPC cells. Latent Epstein-Barr virus (EBV) infection is endemic in this group and the evidence for EBV being the carcinogen is compelling. Other nasopharyngeal tumours.NASOPHARYNGEAL TUMOURS There are four important groups: a) b) c) d) Nasopharyngeal carcinoma (NPC). Adenoids (see Related topics).

NPC often spreads submucosally from the fossa of Rosenmüller so that no nasopharyngeal abnormality is visible although there may be metastatic lymph node disease. It has recently been shown that EBV is associated with all WHO types of NPC. The A2 BW46 allele combination is associated with intermediate term survival while the occurrence of B17 is associated with short term survival. a neck lump or referred otalgia. a bone scan are useful screening tools in the search for distant metastases. . 4th and upper two divisions of the 5th cranial nerves causing diplopia. MRI imaging including a short tau inversion recovery (STIR) sequence to suppress fat clearly defines the tumour margins in soft tissue and will best define the presence and extent of metastatic neck disease. facial hypoaesthesia and headaches.NASOPHARYNGEAL TUMOURS 181 3. pharyngeal. Investigations The diagnosis is made from the history. Plasma antibodies to viral capsid antigen and to early antigens (one of which is an EBV DNAse) are seen. Involvement of the former space causes mandibular nerve paralysis with partial loss of facial. vocal cord. shoulder and tongue paralysis and pain. if symptoms dictate. liver ultrasound and. CT is the investigation of choice to assess skull base and paranasal sinus involvement. Involvement of the latter space containing the cervical sympathetic trunk and the IX-XII cranial nerves causes Horner’s syndrome. NPC usually arises from the fossa of Rosenmuller and may spread by direct extension to involve: • Anteriorly to the Eustachian tube causing a serous otitis media. The polymerase chain reaction to EB virus genome has been used to diagnose NPC in patients with a malignant neck node with an occult primary. palatal and pharyngeal sensation and involvement of the pterygoid musculature causing trismus. palatal. nasal obstruction. • Superiorly through the foramen lacerum to cause paralysis of the 3rd. A ‘blind’ biopsy is not recommended as the specimen obtained may be non-representative. Genetic factors The human leucocyte antigen allele A2 without BW46 or B17 7 is associated with long term survival. examination and special investigations. Seventy per cent of patients will have metastatic lymph node involvement at presentation and in a large Hong Kong series this was the mode of presentation in 40% of patients. • Postero-laterally through the pharyngobasilar fascia to the parapharyngeal and retrostyloid space. Fibreoptic pharyngoscopy is probably the most reliable method of examining the nasopharynx and should be used if a biopsy of the fossa of Rosenmüller is to be obtained under a local anaesthetic. A chest radiograph. Clinical features The majority of patients present with a history of epistaxis. titres of the latter being a significant predictor of tumour relapse after radiotherapy.

N1 Unilateral metastasis in lymph node(s) measuring 6 cm or less in greatest dimension above the supraclavicular fossa. NX Regional lymph nodes cannot be assessed. Europe had traditionally used the UICC system. EBV infection of the nasopharynx is not a regular feature in healthy EBV virus carriers. There is evidence that adjuvant chemotherapy reduces loco-regional relapse and significantly improves prognosis in NPC (actuarial five year survival 64% v 42% in radiation alone group). hypopharynx or orbit. infratemporal fossa. Radical neck dissection may control radio-resistant nodes and post-radiation cervical node recurrence. including Hong Kong. Counselling this group on their diet and the need for frequent regular follow-up is recommended.182 OTOLARYNGOLOGY Staging Several staging systems have been developed for NPC which has made it difficult to compare treatment results using differing modalities and results between centres. In high risk areas screening nasopharyngeal biopsies for viral genomes is useful for determination of high risk individuals. The 5-year actuarial survival is greater stage for stage in WHO type 2a and 2b patients compared to those with WHO type 1 histology. NPC and in particular undifferentiated NPC is highly radiosensitive so a neck dissection is indicated only for radiotherapy failures even if patients present with N3 disease. Prevention 1. Management Radiotherapy using a field which includes the nasopharynx. N2 Bilateral metastasis in lymph node(s) measuring 6 cm or less in greatest dimension above the supraclavicular fossa. T4 Tumour with intracranial extension and/or involvement of cranial nerves. the sphenoid and posterior ethmoid sinuses. N0 No regional lymph node metastasis. T2a: without parapharyngeal extension. the Ho system. North America the AJCC system and Asia. and posterior orbit is the treatment of choice. N3b Metastasis in lymph node(s) in the supraclavicular fossa. In selected patients. Surgery plays a limited role in the treatment of NPC. The consensus view now is to irradiate the neck bilaterally to reduce the incidence of future neck node metastases. In 1997 the 5th Edition of the AJCC Cancer Staging Manual brought the AJCC into line with the UICC and their staging is: T1 T2 Tumour confined to the nasopharynx. salvage surgery may be indicated for nasopharyngeal recurrence. skull-base. N3a Metastasis in lymph node(s) greater than 6 cm in diameter. T3 Tumour invades bony structures and/or paranasal sinuses. . Tumour extends to soft tissue of oropharynx and/or nasal fossa. T2b: with parapharyngeal extension (parapharyngeal extension denotes postero-lateral infiltration of tumour beyond the pharyngo-basilar fascia).

is currently undergoing Phase 1 trials. meningocele). It occurs predominantly and perhaps exclusively in young adult males. . T-cell lymphoma. bimonthly for the second year. arises from the posterolateral wall of the nasal cavity and the superolateral nasopharyngeal wall. teratomas). Infectious mononucleosis. parasellar region. neuroectodermal (encephalocele. cavernous sinus and orbit may also occur. Clinical features The tumour expands to erode or compress surrounding fissures. A high index of suspicion for any nasopharyngeal mass is essential because angiofibroma should not as a rule be biopsied. chordoma). Other nasopharyngeal tumours • Non-Hodgkin’s lymphoma. often with large endothelial spaces. Other EBV associated disease • • • • Burkitt’s lymphoma (a monoclonal B cell non-Hodgkin’s lymphoma). the greater wing of the sphenoid and the skull base foramen. If they are disease free then for most cancers they may be considered cured (adenoid cystic carcinoma and malignant melanoma are notable exceptions). Angiofibroma This histologically benign tumour comprising fibrous tissue with a variable proportion of vascular tissue. expanding superiorly to erode the pterygoid plates. Hodgkin’s lymphoma. a major target for the virus-neutralizing antibody response.NASOPHARYNGEAL TUMOURS 183 2. In particular it must not be confused with a large adenoid pad. Anterosuperior expansion into the nasal cavity. dysontogenetic (craniopharyngeoma. through the pterygomaxillary fissure and into the infratemporal fossa. foramina and tissues. The commonest symptoms are epistaxis and nasal obstruction. • Extramedullary plasmacytoma (predilection for the nasopharynx and paranasal sinuses). paranasal sinuses. • Paediatric nasopharyngeal tumours: ectodermal (dermoids. every three months for the third year and six monthly for the fourth and fifth years post treatment. A vaccine based on the EBV envelope glycoprotein GP340. Many head and neck units will continue to follow patients annually for another five years because such patients are at significant risk of developing a second primary cancer. Presenting signs are similar to NPC except there is a smooth mass filling the nasopharynx on endoscopic or mirror examination. It may expand laterally into the pterygopalatine fossa. The sphenopalatine foramen is always involved and may be the specific site of tumour origin. Follow-up and aftercare All patients with treated head and neck cancer must be reviewed monthly for the first year.

Raslan WF. Sanguineti G et al. Second Consensus. 1995. Cancer. Related topics of interest Adenoids. Induction chemotherapy followed by radiotherapy versus radiotherapy alone in patients with advanced nasopharyngeal carcinoma: results of a matched cohort study. a craniofacial approach are those most widely advocated and these may need to be combined with an infratemporal approach. Large vascular tumours require digital subtraction angiography to define the important feeding vessels. Serological markers in the diagnosis of histopathological types of nasopharyngeal carcinoma. ethmoid and sphenoid sinus endoscopic approaches compare favourably with external approaches with significantly reduced morbidity. Janecka IP. For tumours where involvement is limited to the nasal cavity. Reddy SP. . 19:39–399. Effective Head and Neck Cancer Management.184 OTOLARYNGOLOGY Investigations and treatment An MRI scan with a STIR sequence is the investigation of choice to define the extent and vascularity of the tumour. p. Cervical lymphadenopathy. Surgery is the treatment of choice for all but the smallest tumours as they may continue to expand and are typically poorly radiosensitive. 79: 1279–1286. 2000. 1997. Glisson BS. Fagan JJ. Geara FB. 1997. Nasopharyngeal angiofibromas: selecting a surgical approach. Gooneratne S et al. 29. European Journal of Surgical Oncology. Wilson J (ed). 16:103–108. p. American Journal of Otolaryngology. Carrau RL. Head Neck. 15:357–360. Prognostic significance of keratinization in nasopharyngeal carcinoma. These should be embolized 1–2 days pre-operatively. Depending on tumour extent a mid-facial degloving or. 8. Further reading Sam CK. Pathmanathan R. if the cribriform plate is involved. British Association of Otolaryngologists. nasopharynx. Snyderman CH. 1989. Head and Neck Surgeons. Prasad U.

Radical neck dissection is considered to be the standard basic procedure. The operation may be required to remove the nodes alone. The advantage of using radiotherapy in these cases is that it precludes the need for surgery.NECK DISSECTION A primary carcinoma arising from the upper aerodigestive tract may ultimately drain into the lymph nodes of the neck. The prognosis for the patient regardless of the site of the primary tumour is worse if there are cervical lymph nodes involved at presentation. or it can be performed in continuity with removal of the primary tumour as an en bloc resection. for the foreseeable future it is likely that both these terms will continue to be used. Only 30–40% of such patients will survive longer than 5 years. Modified radical neck dissection. which form an efficient barrier to the further spread of the disease. (a) Supraomohyoid neck dissection. Extended radical neck dissection involves removal of additional lymph node groups or nonlymphatic structures relative to the radical neck dissection (i. It is suggested that this term be used in preference to functional neck dissection. Radical neck dissection. (c) Lateral neck dissection. 3. which should be abandoned. Broadly speaking. The oncologist has two effective treatment modalities for neck node metastases in radiotherapy and surgery. which can be kept in reserve for the treatment of any recurrence. .e. and all others represent one or more alterations to this procedure. Selective neck dissection. 2. (b) Posterolateral neck dissection. Modified radical neck dissection involves the preservation of one or more non-lymphatic structures routinely removed in radical neck dissection. Selective neck dissection involves the preservation of one or more lymph node groups routinely removed in radical neck dissection. a superior mediastinal dissection in patients with subglottic or cervical oesophageal tumours). radiotherapy will only be effective in the curative treatment of cervical lymph node metastases if they are less than 2 cm in diameter. Classification The classification below is suggested by the American Academy’s Committee for Head and Neck Surgery and Oncology. (d) Anterior compartment neck dissection. However. 1. Patients who have larger nodes are less likely to be cured by radiotherapy and must be treated surgically.

2. poor nutritional status). Complications of radical neck dissection 1. The jugular vein preservation is of great importance when bilateral neck dissections need to be performed. marginal mandibular branch of the facial. hypoglossal. but the main advantage from this procedure is that the risk of frozen shoulder (due to accessory nerve resection) is avoided. middle and lower jugular (deep cervical). • Recurrence in the glands or skin. Extended radical neck dissection. Intermediate. 3. the midline anteriorly and the anterior border of the trapezius muscle posteriorly. . Modified radical neck dissection This operation consists of a monobloc removal of the cervical lymph nodes from levels I through to V as with a radical neck dissection. • Haemorrhage (from either end of the internal jugular vein or other ligated vessel). sympathetic trunk. and the posterior triangle group. brachial plexus). Rupture of the carotid artery (may be a sequel to wound breakdown). previous radiotherapy. lingual. Radical neck dissection This operation refers to the removal of lymph nodes in the anterior and posterior triangles extending from the inferior border of the mandible superiorly to the clavicle inferiorly. • Nerve palsies (phrenic. the accessory nerve or the sternocleidomastoid muscle. upper. There is preservation of any one or all of the following structures: internal jugular vein. • Chyle leak (if the thoracic duct has been inadvertently damaged). The submandibular gland. Immediate. Late. Modified radical neck dissection is considered to result in regional control rates similar to those achieved by radical neck dissection as long as patients are carefully selected (patients with mobile nodes not greater than 3 cm in diameter and no more than 3 in number). • Frozen shoulder (less likely to occur if the cervical nerve branches of C3 and C4 are preserved as they pass under the fascia of the floor of the posterior triangle).186 OTOLARYNGOLOGY 4 . Wound infection. Cerebral oedema (after a synchronous or staged bilateral neck dissection). vagus. spinal accessory nerve. internal jugular vein and sternocleidomastoid muscle are also removed. The cervical lymph node groups routinely removed are as follows: submental and submandibular. Wound breakdown (poor surgical technique. diabetes. • • • • • Facial oedema.

Usually applied for skin tumours such as melanoma and skin adnexal tumours (levels II. though it never returns to its normal level. Related topics of interest Cervical lymphadenopathy. Neck dissection. Oral cavity carcinoma. III and IV. Surgery probably does not influence the natural history of the disease. Archives of Otolaryngology and Head and Neck Surgery. 2000. . Current Opinion in Otolaryngology and Head and Neck Surgery. 138. but when the second side is tied there is a tenfold increase in pressure. Thus for patients with NO disease the following procedures remain an option: 1. British Association of Otolaryngologists. p. Laryngeal carcinoma. Posterolateral neck dissection. 197.NECK DISSECTION 187 Selective neck dissection The selective neck dissections are based on a knowledge of the distribution of nodal metastases in the different primary sites. Removes the nodes around the visceral structures in the midline (level VI) and is usually indicated for thyroid cancer. Supraomohyoid neck dissection. 1: 114–119. be nursed propped up in the bed. but univariate analysis demonstrates a reduced 5-year survival to around 5%. p. Anterior compartment neck dissection. The most critical period is the first 12 hours postoperatively. and may require an infusion of mannitol (500 ml of 10% mannitol over 4 hours). Second Consensus. p. IV and V). For cancers of the larynx and hypopharynx the commonest node levels are II. The most serious complication is that of raised intracranial pressure. Lateral neck dissection. 4. Further reading Robbins TK. 1993. p. 2. Bilateral synchronous neck dissection carries a significant morbidity and a mortality of about 3%. Oral cavity tumours commonly metastasize to levels I. The patient should have a temporary tracheostomy. Over the following 8–10 days after the operation. 3. Supraglottic carcinoma with bilateral glands is an exception and can still have a reasonable prognosis. Standardising neck dissection terminology. Many of the complications can be reduced by either staging the procedure with an interval of 6 weeks or longer or performing a modified procedure on the opposite side to preserve the internal jugular vein. Oropharyngeal carcinoma. Robbins TK et al. III. This is because when bilateral disease is present at least one set of nodes is usually of greater diameter than 6 cm and fixed. Hypopharyngeal carcinoma. Head and Neck Surgeons. Wilson J (ed). 117:601–605. Effective Head and Neck Cancer Management. p. 29. the intracranial pressure tends to fall. Bilateral neck dissection The presence of bilateral neck nodes is not an independent poor prognostic sign. 1991. 124. II and III. 203. Ligation of one internal jugular vein results in a threefold increase in the intracranial pressure.

just anterior to the sternomastoid but above the hyoid bone. The parapharyngeal space is a potential space immediately lateral to the oropharynx and nasopharynx. The submandibular space is bound by the mucosa of the floor of the mouth superiorly and by the mylohyoid muscle and deep fascia investing the submandibular gland inferiorly. both complications of acute suppurative otitis media. have been previously described as has peritonsillar abscess (see Related topics). It is bounded posteriorly by the styloid process and the anterior wall of the carotid sheath.NECK SPACE INFECTION Anatomy Understanding neck space infections is straightforward but requires some anatomical knowledge. 1. An abscess behind this fascia cannot extend below this level unless the fascia is breached. That portion behind the pharynx is the retropharyngeal space. The infratemporal fossa therefore is equivalent to the prestyloid compartment of the parapharyngeal space. 3. It is emphasized there is no anatomical barrier preventing an abscess tracking inferiorly into the superior and posterior mediastinum. The pre-vertebral fascia arises from the base of skull in front of the atlas and inserts into the body of T3. Neck space infections Citelli’s abscess and Bezold’s abscess. In the pre-styloid compartment a collection may extend as far forward as the fascia surrounding the submandibular gland. The infratemporal fossa lies beneath the base of skull between the side wall of the pharynx and the ascending ramus of the mandible. Immediately anterior to the pre-vertebral fascia is a potential space extending from the skull base to the diaphragm. the styloid process dividing it into an anterior or pre-styloid and a posterior or post-styloid compartment. 2. The latter contains the carotid sheath. which is firmly attached on its lateral aspect to the investing layer of deep fascia on the deep aspect of sternomastoid but has only loose areolar tissue lying medially and posteriorly. 4. Infection may therefore spread from the prestyloid to the post-styloid compartment by passing medial to the carotid sheath or from the retropharyngeal space to the post styloid compartment (and vice versa) by passing posterior to the carotid sheath. . although the inflammatory reaction usually localizes the abscess to the retropharyngeal space. 5. An abscess in the post-styloid compartment may track further laterally to point just behind the posterior aspect of sternomastoid. anteriorly by the posterior wall of the maxilla and superiorly by the infratemporal surface of the greater wing of the sphenoid.

Occasionally collapse will cause acute spinal cord compression. Treatment It has been suggested that in the absence of airway distress. Older children have fewer retropharyngeal nodes and adults have only the node of Rouviere. Symptoms mimic laryngotracheobronchitis and acute epiglottitis. internal jugular vein thrombosis and mediastinitis. Suppuration of retropharyngeal nodes occurs after an upper respiratory tract infection (URTI) from lymphatics draining infected tonsils. A positive result does not distinguish between tuberculosis and atypical mycobacterial infection. A lateral neck radiograph shows prevertebral soft tissue shadowing and a rarified vertebral body which may be wedge shaped through collapse. teeth. Investigations An inspiratory lateral soft tissue neck radiograph. A progressively painful and tender neck with limitation of movement is the usual presentation. have stertor or dysphagia. Mastoiditis or a pharyngeal foreign body are unusual causes. An expiratory radiograph in a normal child can also cause widening of the retropharyngeal soft tissues so the X-ray must be interpreted as part of the overall clinical picture before treatment decisions are made. The neck is held rigidly and may become hyperextended. The child may need to remain on ICU for 24–48 hours until the retropharyngeal soft tissue swelling settles. even with a correct diagnosis. might cause rupture of the abscess with inhalation or tracking of the abscess into the mediastinum. but it may allow empirical anti-tuberculosis treatment to be instigated while the culture and sensitivity result is awaited. will show the widened retropharyngeal space and narrow oropharyngeal airway. the neck extended to prevent the retropharyngeal soft tissues causing a pseudomass. It has potentially life threatening complications including internal carotid artery rupture. pharynx or paranasal sinuses although occasionally the source is an unsuspected foreign body.NECK SPACE INFECTION 189 Prevertebral abscess This is rare today and occurs in adults from tuberculosis of the cervical spine. Aspirating the abscess allows a sample to be subjected to a Z-N stain. Retropharyngeal abscess The overwhelming majority of cases arise in children less than four years old. The condition occurs in adults when a prevertebral TB abscess ruptures through the prevertebral fascia. It is safer therefore not to examine the throat which. . is highly suspicious of a retropharyngeal or retrotracheal abscess. intravenous antibiotics and close observation may obviate the need for incision and drainage of the abscess in the tonsillectomy position. although in the latter case the history is longer. requiring urgent drainage of the abscess and cord decompression. The attachment of the fascia limits the inferior extent to the vertebral body of T3. The child becomes increasingly toxic and may dribble. Parapharyngeal abscess Sixty percent arise from tonsillitis or peritonsillitis and thirty percent from an abscess of the root of the lower third molar which lies below the mylohyoid line. An increase in the retropharyngeal soft tissue density of more than 7 mm or 14 mm in the retrotracheal area.

Incision and drainage is necessary if there is not a rapid response to intravenous antibiotics or if the airway is becoming precarious. The tongue is pushed posteriosuperiorly and there is trismus and dribbling. Treatment If the airway is not in immediate danger fine-needle aspiration of the abscess and intravenous antibiotics are usually adequate. hot. swollen and tender. Contemporary management of deep space neck infections. the choice of antibiotics being similar to retropharyngeal and parapharyngeal abscess. Flanary VA. either co-amoxyclav or a broad spectrum penicillin/cephalosporin and metronidazole are the combination of choice. Further reading Last RJ. Otolaryngology and Head and Neck Surgery. 116:16–22. These may obviate the need for formal incision and drainage. 38:263–271. There may be no history of dental pain if the root is close to the inner table of mandible which gives way early. This is usually preceded by the insertion of a nasopharyngeal tube to secure the airway. It lies most commonly behind the posterior aspect of the upper or middle third of the sternomastoid because infection most commonly drains from the pre-styloid to the post-styloid compartment and there-after laterally. Clinical features Floor of mouth oedema secondary to cellulitis can progress rapidly to endanger the airway. soft palate oedema. The remaining cases are secondary to tonsillitis. A mixed population of aerobic and anaerobic organisms are usually present. often torticollis. Gidley PW. red. There is a hot. . 1997. Stiernberg CM.190 OTOLARYNGOLOGY Clinical features These are similar to a peritonsillar abscess. London: Longman. Pediatric deep neck space infections: the Medical College of Wisconsin experience. Submandibular abscess (Ludwig’s angina) In over 80% of patients infection arises from a root abscess of the lower premolars or the first and second molars. tender swelling which may be firm or fluctuant or diffuse. International Journal of Pediatric Otorhinolaryngology. Conley SF. Treatment Repeat fine needle aspiration of the abscess and intravenous antibiotics. The submandibular region is red. Anatomy: regional and applied. 1997. and the tonsil is pushed medially. There is trismus. Ghorayeb BY. 1999. 7th edn.

. p. p. 330. 311. Paediatric airway conditions. Tonsil diseases. 5. Stridor and stertor.NECK SPACE INFECTION 191 Related topics of interest Acute otitis media. 232. p. p.

recreational. discos and personal stereos. with increasing noise levels above 90 dB(A). Clinical features TTS may be perceived as ringing in the ears (tinnitus) following excessive noise exposure. Occupational deafness is a compensable disease and legislation exists to protect the employee (Health and Safety at Work Act). and subsequently to the OHCs in rows 2 and 3 and the inner hair cells. such as shooting. However. Initially noise exposure will lead to temporary threshold shift (TTS). he is statutorily obliged to provide a hearing protection programme to include hearing protection. such as factory machinery. Gender and increasing age appear to have an influence on susceptibility. When PTS becomes symptomatic the first complaint is usually reduced understanding for . A doubling in sound intensity corresponds to an increase of only 3 dB.NOISE-INDUCED HEARING LOSS Aetiology and background The ear is a sound-sensitive organ but can be damaged by excessive noise levels. while a 10-fold increase in intensity corresponds to an increase of 10 dB. Motorcycling and car airbags are both recently recognized causes of noise-induced hearing loss (NIHL). Excessive noise can arise from a variety of sources: occupational. Pathology Biological variability means that individuals are not affected equally by the same noise exposure. At the second action level of 90 dB(A). Such screening is a requirement of any hearing protection programme. In the UK the first action level is 85 dB(A) for an 8-hour working day. There are no obvious pathological changes in TTS and the problem is probably due to metabolic ‘exhaustion’ of the hair cells of the cochlea. home power tools. The audiometric hearing loss tends to parallel the loss of hair cells. at which point an employer is obliged to monitor the hearing levels of his work force and to monitor noise levels at the work place. Therefore small increases in noise exposure recorded in dB expose the cochlea to large increases in sound energy. monitoring and efforts to reduce sound levels at source. Permanent threshold shift (PTS) is frequently asymptomatic initially and is often found on routine screening audiometry carried out in the workplace. initially to the outer hair cells (OHCs) of row 1. a recoverable phenomena. building sites and high-impact tools. With increasing and repeated noise exposure there is permanent direct mechanical and metabolic damage. a greater proportion of the exposed population will exhibit pathological changes. Damage also occurs to the supporting pillar cells and the stria vascularis.

Further reading King PF. Investigations A good history is the key to diagnosis and is essential in personal injury medicolegal cases in order to provide apportionment of disability if more than one type of noise exposure has occurred. and as such a scheme exists to calculate the disability and hence the amount of compensation. any conductive loss and the type of audiogram. further deterioration must be prevented by adequate protective measures or better still. high-tone sensorineural hearing loss or intermittent tinnitus. especially when there is background noise. In essence this involves averaging the hearing thresholds for each ear for the frequencies of 1. to minimize disability. There are increasing research reports of the use of pharmacological agents to protect the cochlea metabolically from the effects of noise. and a figure for the disability is finally reached. Unfortunately tinnitus is a frequent accompanying symptom in noise induced hearing loss. Examination will reveal normal tympanic membranes (unless the patient has had previous middle-ear disease) and the audiogram will often show a dip at around 4–6 kHz in the early stages. Guidelines for Medicolegal Practice. 2 and 3 kHz. 1999. Follow-up and aftercare Continuing advice and review by a hearing therapist is recommended to minimize disability. Current Opinion in Otolaryngology Head and Neck Surgery. regarding the hearing loss and frequent tinnitus. 1992. London: Whurr. Personal injury cases are argued on their individual merits. preferably from a hearing therapist. A hearing aid may be required. As it becomes more severe the patient complains more of being hard of hearing. 7:266–273. It is also essential when assessing any claimant with NIHL to consider alternative explanations for the hearing loss. This may become exaggerated as exposure continues. e. Coles RRA. until eventually there is flattening of the audiogram as sensorineural damage progresses. age. Allowance is then made for any difference between the two ears. Robinson DW. Awareness of the potential hazards of noise will allow prophylactic measures to be taken both at work and recreationally. Cerebellopontine angle tumours may produce a unilateral asymmetrical. Lutman ME. McFadden SL.NOISE-INDUCED HEARING LOSS 193 speech. Recent advances in understanding and preventing noise-induced hearing loss. Counselling is helpful. the use of earplugs and muffs. . Management: medicolegal Occupational noise-induced hearing loss (NIHL) became a compensable disorder in 1975. avoidance of further noise exposure.g. nonsyndromic hereditary and degenerative causes are not uncommon. Henderson D. once diagnosed. so investigation to exclude this cause is sometimes necessary. Assessment of Hearing Disability. Management Damage to the cochlea caused by noise is cumulative so that.

p.194 OTOLARYNGOLOGY Related topics of interest Acoustic neuroma. 1. . p. Non-organic hearing loss. Impedance audiometry. 254. p. Pure tone audiogram. p. 128. 194.

the Stenger test (see Clinical assessment of hearing. In the child. The pure tone audiogram itself may be performed in an erratic and hesitant fashion. 45). In the latter group this psychosomatic symptom represents a cry for help in response to some current stressful event. Pure tone audiometry. In the truly deaf patient pure tone audiometry reveals consistent results. 2. Investigations A plethora of tests exist to try and distinguish non-organic from organic hearing loss. A patient with a genuine unilateral hearing loss would perceive the bone-conducted stimulus in the normal cochlea and report the perception of sound. The stapedius reflex threshold normally varies from 70 to 95 dB above the pure tone threshold. There may be recruitment. in the good ear. These can be used as part of the clinical assessment in cases of apparent unilateral hearing loss. In the former group the patient usually exaggerates an existing hearing loss in an effort to improve any compensatory payment. although it may not always be possible to identify the stressor.NON-ORGANIC HEARING LOSS Non-organic hearing loss (NOHL) is a condition in which a patient consistently displays an apparent auditory deficit. Tuning forks. when no true hearing loss exists.g. a non-organic component must be excluded. One should suspect a NOHL when pure tone responses are inconsistent or when the patient denies hearing. Those patients who have some degree of psychological upset often appear completely unconcerned about the hearing loss but are very often accompanied by an extremely concerned carer. 3. p. or exaggerates a real hearing loss. The patient appears to hear much better than the subsequent audiogram would suggest (but beware of lip readers). Even then there is usually . Impedance audiometry. ototoxic drugs or trauma). it has been estimated to occur in up to 25% of cases. Patients complaining of a unilateral hearing loss may deny any hearing of a tuning fork placed on the mastoid process of the affected side. which can also be performed using an audiometer. The prelimin-ary clinical investigation may reveal some inconsistencies which suggest the diagnosis. the underlying hearing is usually normal. in all patients who are pursuing a financial claim. Clinical assessment The diagnosis of NOHL depends primarily on a high index of clinical suspicion. a sound over 70 dB above the threshold applied to the bad ear. so this is not invariably the case. 1. Unfortunately. or in a child with psychological disturbance. This condition is usually encountered either in an adult. particularly financial claims and in children without obvious pathology. e. in whom there is an ongoing claim for compensation as a result of ototrauma (hearing loss from noise exposure.

910–931. Speech audiometry. p. A hearing aid may be provided for its placebo effect when there is great distress on the part of the patient or carers. and an honourable escape route is provided. 26:347–350. Impedance audiometry. 1992. 78. slow down or shout. as in medicolegal cases. If the patient is feigning deafness then the delayed speech feedback will alter the reading pattern causing the patient to stammer. Fortunately. Follow-up is only required to document the return of normal hearing. disturbed. p. Electrocochleography can be used. p.196 OTOLARYNGOLOGY at least 20 dB between the reflex threshold and the pure tone threshold. . Delayed speech feedback. electric response audiometry will be required. p. Cortical responses are preferred to brainstem evoked responses as they provide precise threshold levels and establish integrity of the entire auditory pathway. 128. In: Beagley HA (ed. successful. 3rd edn. Geoghegan PM. Patients often find it more difficult to exaggerate their impairment to the same extent in speech as in pure tone audiometry. Management The aims in management are first to recognize that there is a non-organic hearing loss and thereafter to ascertain the true auditory thresholds. If there is a genuine deafness the patient will be able to read without pausing. 2. Hearing in Children. Patients pursuing a financial claim are well aware of their actions. Speech audiometry. Once it is indicated to a patient that the true thresholds are suspected. Confrontation is rarely. Strong reassurance that there is nothing serious present and that the hearing will improve in time is usually all that is required. the recording being delayed by milliseconds. 1981. If knowledge of the auditory thresholds is required with some precision. if ever. Pure tone audiogram. 4. Related topics of interest Clinical assessment of hearing. Brooks DN. Evoked response audiometry. and compensated accordingly. 254. 45. Non-organic hearing loss in young persons: transient episode or indicator of deep-seated difficulty. group the condition is usually short lived. Northern JL. but this technique is invasive and gives no information about the central auditory pathways. 301. p. Any true hearing loss can then be treated on its merits. Baltimore: Williams & Wilkins. as the stressing event disappears or the patient develops appropriate coping strategies. Non-organic hearing loss in adults. Downs MP. Noise-induced hearing loss. The patient is asked to read aloud from a book. 5. If the thresholds are within 20 dB or less than a NOHL is likely. 6. Follow-up and aftercare In severe or prolonged cases (up to 20%) appropriate psychiatric referral may be required. including the provision of a hearing aid if required. rarely lasting more than a few weeks or months. Vol. 1984. in the younger. This is often useful in making the diagnosis. p.) Audiology and Audiological Medicine. the NOHL will often disappear on repetition of testing. Evoked response audiometry. 192. British Journal of Audiology. Oxford: Oxford University Press. The voice is recorded and played back into the bad ear via headphones. Further reading Alberti P.

Tongue mobility and dental hygiene should also be noted. . Tumours of the anterior floor of mouth and alveoli tend to spread to the submandibular nodes.ORAL CAVITY CARCINOMA The oral cavity consists of the buccal mucosa. which are present in nearly a third of patients at the time of presentation. salivary gland and connective tissue origin occur in the oral cavity. but the incidence of occult metastases is high (35%). Other aetiological factors include smoking tobacco. but in India it accounts for more than 40% because of the common practice of chewing betel quid containing tobacco. and those from the posterior oral cavity tend to metastasize to the jugulodigastric nodes. Second primary tumours occur in up to 30% of patients with oral cavity carcinoma. They are most commonly found in the oral cavity. Clinical features The patient may complain of a painful ulcer. The incidence of squamous cell carcinoma of the oral cavity varies worldwide. The commonest sites are the lateral border of the tongue and the floor of the mouth. which are in the oropharynx. Most patients are over the age of 40 years with a peak incidence in the sixth and seventh decades. Alveolar tumours may interfere with dentures. a warty growth. On examination the site. sarcomas and melanomas. Pathology Although benign tumours of epithelial. mucoepidermoid tumours. difficulty in eating and speaking. particularly in a pipe. the upper and lower alveoli. Over 90% of the malignant tumours are squamous cell carcinoma. The remainder include adenoid cystic carcinoma. the oesophagus and in the lungs. the majority are malignant. It does not include the posterior third of the tongue. Some tumours present with no nodes palpable (NO). halitosis and. The male to female ratio is 2:1. The tongue has a well-developed lymphatic drainage. but some anterior tumours may spread directly to the jugulo-omohyoid nodes. Tongue tip tumours spread to the submental lymph nodes first. the hard palate. the anterior twothirds of the tongue and the floor of the mouth to the anterior tonsillar pillars. There is also an increased incidence in patients with cirrhosis of the liver. but also occur in other sites in the head and neck. soft palate or tonsils. and high alcohol consumption. later. tumours of the lateral border of the tongue spread to the jugulodigastric nodes. They usually present as an ulcer but may protrude as an exophytic-type lesion. The neck should be examined for nodal metastases. In the UK it accounts for less than 2% of all malignancies. size and extent of the tumour should be assessed.

Isotope bone scans are very sensitive for the presence of mandible invasion. the presence of any intercurrent disease and their general condition. and patients may require a full dental extraction prior to treatment. exclude a second primary. can then be planned. TNM classification Tis T1 T2 T3 T4 Carcinoma in situ. including the feasibility and nature of a surgical resection. Primary radiotherapy should not be used to treat tumours involving the mandible as later excision of the bone may lead to osteoradionecrosis. Nutritional status and the need for percutaneous gastrostomy should be assessed. The patient is spared the ordeal of surgery and maintains good oral function. They should also be referred to a speech therapist for counselling in respect of their postoperative speech and swallowing rehabilitation. Small tumours of the alveolar margin can be treated by a marginal mandibulectomy. the extent of local and distant spread. loss of taste and mucositis can be troublesome side-effects. xerostomia. but some quality of life studies support surgery as the primary modality for these lesions. Tumour more than 2 cm but less than 4 cm in its greatest dimension. can be repaired with a radial forearm free flap. All patients should have an examination under anaesthetic to obtain a biopsy. Management The management of all patients depends on the site and size of their tumour.198 OTOLARYNGOLOGY Investigations An orthopantomogram may demonstrate involvement of the lower alveolus by the appearance of a motheaten rim or an opacity of the normal lucent dental canal A CT scan is also useful to delineate the extent and local spread of these tumours. check the neck for nodes and stage the disease. It is important to remember that the surgery required can impair the functions of swallowing and speech besides its effect on the appearance of the patient. 2. evaluate the tumour. Tumour 2 cm or less in its greatest dimension. . T3 and T4 tumours. Tumour with extension to bone. Oromandibular function impairment is often quoted as an argument against surgery. A chest radiograph is mandatory to exclude lung metastases. Larger tumours of the tongue need a partial or total glossectomy. skin. they are not specific and consequently there is a significant false positive rate. A combination of external beam and implants can be used. Small tumours can be resected transorally using a cutting diathermy or CO2 or KTP laser with primary closure or closure with a quilted split-skin graft. The disadvantages of external beam radiotherapy are: it cannot be used again at the same site. 1. salvage surgery for radiotherapy failure has a low survival and high morbidity. removing up to half of the tongue. Therapy. Surgery is as efficient as radiotherapy in the treatment of T1 and T2 tumours. Prior to treatment all patients should see a dentist/prosthodontist to assess the status of the teeth. MRI scans are not good for illustrating bone invasion but they are particularly useful in the soft tissue delineation of tongue tumours. With some of the larger T2 tumours a radial forearm free flap may be necessary. Radiotherapy can also be used for T1 and small T2 tumours. However. If more than half of the tongue is removed it should be reconstructed by a pectoralis major myocutaneous flap or a rectus abdominus free flap. A partial glossectomy. The aim of surgery is to resect the disease while maintaining maximal function and cosmesis. T1 and T2 tumours. etc. Tumour more than 4 cm in its greatest dimension. muscle.

1996. Irradiation to both sides of the neck or bilateral neck dissections with preservation of one internal jugular vein are possible. 4:98–105. Zaretsky L. If much of the anterior segment of the mandible is removed the soft-tissue and bony defect should be reconstructed with a composite osteocutaneous free flap. Because of lymphatic crossover. surgical excision of the primary tumour and modified radical (preferable) or radical neck dissection is the treatment of choice. elective treatment to the first echelon nodes should be given either by radiotherapy or selective neck dissection. Further reading Wildt J. the prognosis is poor. two or more positive nodes and whenever there is extracapsular spread. 4. Patients should have a monthly outpatient review for the first 6 months and then every 2 months for 6 months. Tongue lesions seem to metastasise to levels II and III more often. Most surgeons advocate the use of postoperative radiotherapy. This is effective in reducing primary recurrence and has been shown to improve survival when: there are positive margins. consideration should be given to treatment of both sides of the neck. to be given within 6 weeks of surgery. but the decision to treat other than for palliation should be carefully considered. Neck nodes. infirm patients who are in poor general condition. especially with anterior oral cavity lesions and those located in the midline. perineural or intravascular invasion. If the patient has palpable neck node metastases. Level IV should therefore be resected for these tumours (‘extended’ supra-omohyoid neck dissection). Clinical Otolaryngology. Follow-up and aftercare The highest mortality is in the first 2 years after diagnosis. The donor sites of grafts and flaps should be checked until they have healed. In some cases no nodes are palpable (NO) but the incidence of occult metastases is high (35%). In addition. 2:343–347. 1994. or who have severe intercurrent disease. Current Opinion in Otolaryngology and Head and Neck Surgery. large primary tumours (large T2. poor histological differentiation. The radial forearm or composite fibula flap are usually used. A supra-omohyoid neck dissection (levels I. The nutritional status and weight of the patient should be monitored. The risk of a second primary tumour should be remembered. to radical treatment These patients should have supportive nursing care and when necessary adequate analgesisa for pain relief. 1989. Special considerations in management of the mandible for cancer of the oral cavity.ORAL CAVITY CARCINOMA 199 preserving the outer cortex of the mandible. Therefore in all (but the very smallest T1 tumours) cases of oral cancer. and speech therapy may be appropriate in some cases. 14:10–13. but a partial mandibulectomy may be required. Current Opinion in Otolaryngology and Head and Neck Surgery. Some patients who have a large tumour with advanced local spread or with distant metastases will not be suitable for curative treatment. The oral cavity and neck should be carefully examined for signs of recurrent disease. T3 and T4 lesions do badly when treated by radiotherapy alone. Shindo ML. II and III) is the usual procedure. Soft tissue reconstruction of the oral cavity and pharynx. 5. it may be inappropriate to subject elderly. If there is going to be a recurrence it is likely to be in the first year. et al Squamous cell carcinoma of the oral cavity: a retrospective analysis of treatment and prognosis. . T3 and T4). 3. If the patient has bilateral neck node disease. DeLacure M. Intense prosthodontic rehabilitation should be given where appropriate. then three monthly for the second year. Postoperative radiotherapy. Palliative treatment.

. 264. Effective Head and Neck Cancer Management. p. Second Consensus. 267. p. Radiotherapy. 2000. Head and Neck Surgeons. British Association of Otolaryngologists. p.200 OTOLARYNGOLOGY Wilson J (ed). Related topics of interest Oropharyngeal carcinoma. 203. Reconstructive surgery.

OROANTRAL FISTULA Definition A fistula is an abnormal communication between two epithelial-lined surfaces. Fractures of the maxilla or penetrating wounds such as a gunshot injury of the hard palate. Neoplasm. A fistula may also follow the search for retained root fragments after a tooth has been broken. 3. foreign bodies. The fistula forms through the tooth socket following a dental extraction. A patient who has previously had inferior meatal antrostomies may notice that air or fluid and food particles can be sucked through the fistula into the nose. The diagnosis can be established by passing a probe through the fistula into the antrum. Biopsy is needed if neoplastic disease is suspected. . the roots of which may penetrate the floor of the antrum. particularly of the first upper molar and second premolar teeth. An oroantral fistula is a communication between the oral cavity and maxillary antrum. The injection of a contrast medium into the defect is helpful in confirming the presence of a fistula in doubtful cases. Purulent discharge may collect in the nose or mouth and a foul smell or taste is often noticed. The incision line fails to heal. especially in the cases of neoplasia. 2. Trauma. Malignant disease of the antrum may occasionally cause erosion into the oral cavity. Its incidence is probably higher than is recognized because many fistulae escape diagnosis following dental extraction and heal spontaneously without complications. Caldwell-Luc operation. signs of erosion by neoplastic disease or infections of the maxillary sinus. Clinical features The patient may complain of symptoms of chronic maxillary sinusitis. Investigations Radiological examination by sinus radiography and orthopantomogram may show retained root fragments. A CT scan will improve delineation. Aetiology 1. Dental extraction. 4.

249. The bare area is then covered by a mucoperiosteal flap. Oxford: Blackwell Scientific Publications. this must be removed or treatment will be unsuccessful. If the fistula has not healed it will need formal surgical closure. Pus should be sent for culture and sensitivity and a generous meatal antrostomy carried out under antibiotic cover in order to aerate the sinus and allow drainage of pus or secretions. When a fistula is discovered later there will nearly always be friable granulation tissue in the tract and possibly an antral infection. Sinonasal tumours. Diseases of the oral cavity. The infection should be treated first.202 OTOLARYNGOLOGY Treatment The important factors determining treatment are the length of time the fistula has been present and the presence or absence of infection. The patient should be reviewed in the outpatient department monthly until healing is complete. If there is a retained root. Stell PM (eds) Clinical Otolaryngology. For those following dental extraction the most satisfactory treatment is immediate suture at the time of the dental treatment. The patient should be reviewed 4 weeks later. If adjacent teeth cause a problem in closure they should be removed. if not present. p. The patient should give consent for this. Further reading Snow GB. Any foreign body must be removed and the bony edges of the alveolus reduced. Related topics of interest Pharyngocutaneous fistula. In: Maran AGD. . Follow-up and aftercare Decongestant nose drops and a broad-spectrum antibiotic should be prescribed for the first postoperative week and the choice revised according to culture results. should be fashioned at the same time as the fistula closure. 1979. The fistula tract is incised circumferentially around the margins of the fistula and turned inwards. Van Der Waal. If there is evidence of chronic sinus infection an antrostomy. p. 363–365. The adjacent buccal mucosa or a palatal flap based on the greater palatine artery may be used. 280.

OROPHARYNGEAL CARCINOMA Boundaries • • • • Roof: oral surface of the soft palate and uvula. 10%: Non-Hodgkin’s lymphoma (NHL). rhabdomyosarcoma. Lateral wall: anterior and posterior tonsillar pillars and the palatine tonsil. Carcinoma >2 < 4 cm at largest dimension. There is a male : female ratio of 5:1 for SCC. smoking and in smokers alcohol (not proven to be a risk factor alone) are risk factors. Betel nut chewing. Thirty per cent of SCC patients will have either a synchronous second primary or will develop a metachronous second primary within 10 years of presentation. The lingual surface of the epiglottis is now classified as being a subsite of the supraglottis (UICC 1997). 2%: Minor salivary gland carcinoma (MSGC). . Pathology • • • • 85%: Squamous cell carcinoma (SCC). Leukoplakia and in particular erythroplakia are pre-malignant. Carcinoma in-situ. 3%: Others e. Carcinoma > 4 cm at largest dimension. of these 50% are adenoid cystic. Most soft palate MSG tumours are pleomorphic adenomas. Staging summary Tx Tis T0 T1 T2 T3 Tumour cannot be assessed. Carcinoma < 2 cm at largest dimension. Anterior wall: posterior third of tongue and vallecula. No primary evident. Posterior wall: from the level of the hard palate to the aryepiglottic folds.g. Most MSGC arises from the lateral wall. Ninety-five per cent of NHL involves the palatine or lingual tonsil.

mandible. T1 and small T2 stage SCC can be treated with radio-therapy as can N1 neck disease. MSGC and SCC require a macroscopic margin of 1–2 cm and clearance must be confirmed by frozen section. prednisolone. 3. odynophagia and muffled speech are common. NHL requires assessment by an oncologist to properly stage the disease. oncovine (vincristine) and prednisolone) is the most commonly favoured. Should the dental canal be involved a partial mandibulectomy is performed with reconstruction using a composite radial . Trismus is a late symptom and suggests pterygoid involvement. Sore throat. VAPEL-B (vincristine. etoposide. Clinical features Twenty per cent of patients present with a neck lump as the only symptom. A panendoscopy under general anaesthesia is necessary to properly assess the hypopharynx. fitness and wishes. To obtain adequate exposure of the lateral oropharynx. e. looking abnormal compared to its partner. The exact site is determined after assessing an orthopantomogram as the incisor and canine roots are often not parallel. With many T4s macroscopic clearance is not possible. Fine needle aspiration cytology (FNAC) of any palpable neck lump. Chemotherapy or radio-therapy may reduce tumour size for clearance to be attempted but this will depend on the patient’s age. An MRI scan with a STIR sequence will accurately define the extent of soft tissue invasion and neck node involvement. Investigations 1. In the relatively unusual event that the lymphoma is very localized. It is preferred to CT scanning. trachea and bronchi for synchronous disease. SCC is either exophytic or ulcerative but with NHL the tonsil is either large and vascular or small and shrivelled. into the pterygoid muscles. 4. number and fixation of any palpable neck lump(s). deep muscle of tongue or/and larynx. hard palate. radiotherapy may be used. Suspicious tongue base lesions always require a deep biopsy as the cancer may be submucosal. level. osteomyelitis and non-union of the plated mandible. adreomycin. Palpating the tumour and the neck is important to assess the extent of infiltration of the primary and to assess the size. If involvement up to and including the mandibular periosteum has occurred an inner table mandibulectomy is performed. Management Most oncologists treat medium and high grade NHL as a disseminated disease and the CHOP regime (cyclophosphamide. hydroxydaunorubicin. One canine and an incisor may need to be extracted at mandibulotomy to ensure the plating screws do not impinge on a root thereby predisposing to a root abscess.g. oesophagus. 2. If a neck lump is not palpable but is defined on MRI or CT imaging FNAC should be performed under either ultrasound or preferably CT guidance. A full head and neck examination is mandatory because of the high incidence of a second primary. A chest X-ray and liver ultrasound are performed as these are the commonest sites for distant metastases. If disease is limited to the tonsil a tonsillectomy is performed in order to obtain macroscopic clearance.204 OTOLARYNGOLOGY T4 Carcinoma extending beyond oropharynx. cyclophosphamide and bleomycin) is a more recent regime favoured by some oncologists. referred otalgia. a stepped paramedian mandibulotomy is necessary in order to preserve the inferior dental nerve. Large T2 and T3 stage disease is treated with surgery.

Effective Head and Neck Cancer Management. Teknos TN. In: Million RR. The pre-epiglottic space in large tongue base cancer is almost certain to be invaded so that the only oncologically safe procedure is a total glossolaryngectomy with oral and pharyngeal reconstruction with a pectoralis major myocutaneous flap. If a recurrence occurs. Rehabilitation so that sufficient fluid and nourishment can be swallowed to maintain homeostasis can take many weeks and in these a percutaneous gastrostomy is preferable to nasogastric feeding. JB Lippincott. Any mucosal irregularity in this region must be biopsied in case there is underlying recurrent disease is. Wilson J (ed). Oropharyngeal reconstruction. 1998. Large posterior wall SCC is rare and is probably best treated by a total laryngopharyngo-oesophagectomy and reconstruction with a stomach transposition. Follow-up and aftercare After surgery swallowing is frequently seriously impaired. T2 tongue base SCC may be excised after a paramedian mandibulotomy by a midline tongue split or via a lateral pharyngotomy after exposing the structures in the post-styloid compartment of the parapharyngeal space. Cassisi NJ. Cassisi NJ (eds) Management of Head and Neck Cancer. The regularity of follow-up is the same for any head and neck cancer and is outlined elsewhere (see Related topics of interest). Bilateral elective neck irradiation or bilateral selective neck dissection (levels I-IV) should be considered. Philadelphia. 6: 268–271. The neck and primary site may be irradiated in N1 neck disease with a small primary. Oropharynx. Head and Neck Surgeons.OROPHARYNGEAL CARCINOMA 205 fore-arm (if less than 10 cm of mandible is taken). Swallowing rehabilitation should be instituted by a speech therapist with a special interest in swallowing as soon as nourishment is allowed by mouth. Postoperative radiotherapy may be required (more than one node involved. 2000. 401–431. Management of the neck In the NO neck. A radical neck dissection is required for N3 disease. a composite fibula or a composite deep circumflex iliac microvascular free flap. A modified radical neck dissection is used for N1 and some N2 neck disease when surgery is the treatment of choice for the primary. 1994. Soft palate oropharyngeal cancer should be irradiated if small but larger tumours require a partial soft palatectomy with reconstruction using a radial forearm fasciocutaneous microvascular free flap which gives the best result in terms of function and cosmesis. extracapsular rupture or positive margins). British Association of Otolaryngologists. T1 and small T2 posterior wall SCC can be irradiated. normally on around the 10th post-operative day. Second Consensus. Further reading Million RR. Strictures at the anastomosic line in those who have had a stomach transposition are unusual but may require repeated dilation. 2nd edn. consideration should be given to elective neck therapy as there is a high risk of occult neck involvement in oropharyngeal disease. Current Opinion in Otolaryngology and Head and Neck Surgery. excision with at least a 1 cm margin may allow reconstruction of the posterior wall with a radial forearm fasciocutaneous microvascular free flap allowing the patient to keep their larynx. .

p. p. Oral cavity carcinoma. . 267. Reconstructive surgery. p. 124. 138. 264.206 OTOLARYNGOLOGY Related topics of interest Hypopharyngeal carcinoma. Laryngeal carcinoma. 197. Radiotherapy. p. p.

IX and Xth cranial nerves) also causes neuralgic type pain. acute otitis media. Malignant otitis externa (pseudomonas infection) and tumours. the external meatus or middle ear. although it is most common in the glossopharyngeal nerve. Anatomy The sensory nerve supply of the external and middle ears arises from many sources. chondrodermatitis nodularis helicis. perichondritis. neoplasms.OTALGIA Otalgia is pain in the ear (earache). Primary otalgia Primary otalgia arises as a result of direct stimulation of the sensory nerves due to otogenic pathology. The upper half receives its supply from the lesser occipital nerve (C2) medially and the auriculotemporal nerve laterally (mandibular branch of Vth cranial nerve). The external auditory meatus and lateral tympanic membrane receive their supply from the auriculotemporal nerve and branches of the facial and vagus nerves (Arnolds nerve). The pain may emanate from the pinna. Pinna. furuncles. predominantly C2 and C3. Secondary (referred) otalgia Referred otalgia may arise from disease in any peripheral territory supplied by the nerves. acute mastoiditis. neoplasms. This condition gives rise to severe lancinating pain arising in the tonsillar fossa or tongue base and radiating deeply in the ear. . Traumatic perforation of the tympanic membrane. The lower half of the pinna receives its sensory supply from the great auricular nerve via the cervical plexus. often induced by talking or swallowing. It is important to remember that otalgia may arise from a primary neuralgia of any of the sensory nerves. 2. myringitis bullosa (Coxsackie B virus infection). may also produce severe pain. Shingles of the ear (herpes zoster oticus—VII. Trauma from ear cleaning. Middle ear. It may be caused by primary disorders of the ear (otological in origin) or may be secondary to disease from other sites in the head and neck which share the same sensory innervation (referred pain). 1. by virtue of involving bone. otitis externa. Haematoma. External auditory meatus. It is a symptom not a diagnosis. Less commonly the pain may be centred in the external auditory meatus and not be induced by throat movement. shingles. lacerations. 3. The medial aspect of the tympanic membrane and middle ear is supplied through the tympanic plexus by the facial and glossopharyngeal nerves (Jacobsens nerve).

• Soft tissue injury. Particular attention should be paid to the tongue base. • Arthritis/cervical spondylosis.208 OTOLARYNGOLOGY Causes A brief list and system of classification for the commoner causes of referred otalgia is given below.g. The examination should include the ears. with both claiming the symptom is in the other’s department. 1. it is worth reconsidering a neuralgia (e. Trigeminal nerve (Vth cranial nerve). 4. Otalgia is common following tonsillectomy. A trial of carbamazepine or amitriptyline may benefit the patient. • Nasopharyngeal disease such as viral infection. a small adenoid cystic carcinoma of the tongue base may not be apparent on examination. This condition may be successfully treated by tympanotomy and section of the tympanic plexus. It is not uncommon to find a small group of patients with otalgia shuttling back and forth between ENT and oral surgeons. • Carcinoma of the larynx and hypopharynx. • Almost any oropharyngeal infective process may lead to otalgia. tonsillitis and quinsy. scans may be appropriate (e. particularly of posterior teeth. Assessment A full history and examination will normally direct attention to the offending part of the head and neck. In cases where doubt exists. Occasionally. • Sinonasal disease and salivary gland disease are uncommon causes of referred otalgia. . the temperomandibular joints. Second and third cervical nerves (C2 and C3). caries and abscess. tumour or post adenoidectomy. Management Appropriate treatment should then be directed at the underlying cause. 3. Glossopharyngeal nerve (IX cranial nerve). such as pharyngitis. and temporomandibular joint dysfunction are probably the commonest non-otological causes of otalgia. and in those in whom there are absolutely no abnormal findings. • Tumours of the tongue base. the neck and the oral cavity. except perhaps some mild clunking of the temperomandibular joint. In such cases. no abnormality can be found even after a thorough examination and further investigation. • Dental disease such as tooth impaction. 2. pharynx and larynx. as pathology here can be catastrophic if overlooked.g. Vagus (Xth cranial nerve). glossopharyngeal neuralgia). but obvious on an MRI scan).

209. 1990. 97. Irving RM. p. Role of tympanic neurectomy in otalgia. Related topics of interest Acute suppurative otitis media. . 5. p. Journal of Laryngology and Otology. p. Otitis externa.OTALGIA 209 Further reading Cook JA. Facial pain. 104: 114–117.

lying on a thin dermal bed containing sweat glands. The secretions of the sebaceous glands keep the stratum corneum water-tight and supple. . usually caused by P. bathing. especially from dirty fingernails. ceruminous glands and sebaceous glands. aeruginosa or occasionally S. Pathology The skin of the EAM comprises in the outer third an epithelial layer containing hair follicles. • Inherited—narrow ear canals and non-atopic eczema. Sweat gland secretions keep the secretion at a pH between three and five which is lethal for most human pathogens. cotton buds and hairgrips. The skin of the bony ear canal lacks appendages and thins from without in. Perichondritis. Furunculosis. Classification 1. parakeratosis and spongeosis. Staphylococcus aureus and non-haemolytic streptococci are unusual. aureus. aureus.OTITIS EXTERNA Definition Otitis externa is an inflammation of the skin of the external auditory meatus (EAM). Infective (a) Bacterial Diffuse otitis externa commonly caused by Pseudomonas aeruginosa. hot. Predisposing factors • Heat. Malignant otitis externa. Usually the EAM is sterile or contains Staphylococcus albus commensals. aureus and Proteus. • Trauma. oedematous and tender ear canal. S. The epithelial reaction consists of vesication. usually caused by S. Erysipelas caused by Streptococcus pyogenes. humidity. swimming. In the acute phase of otitis externa there are dilated dermal blood vessels of increased permeability which cause signs of a red.

Secondary to an acute or chronic otitis media. Plain lateral-oblique and Towne’s projection mastoid radiographs may show mastoid air cell coalescence in acute mastoiditis but in this and furunculosis the mastoid air cells may be cloudy on the lateral view. atopic tendency and previous otological problems should be made. Although the history may provide a pointer towards the diagnosis. On examination erythema is a feature of eczema. for example tonsillitis and sinusitis and preceding symptoms of otitis media should be sought. In the former there is postauricular tenderness localized to a palpable lymph node. Vesication occurs in eczema. Psoriasis. Conditions affecting the ear canal are limited and a diagnosis can usually be made on examination. an infection of the superficial layers of the epidermis. Aspergillus niger Aspergillus fumigatus Candida albicans (c) Viral Herpes simplex Herpes zoster Presumptive in otitis externa haemorrhagica. .OTITIS EXTERNA 211 (b) Fungal (c) Viral Impetigo. pyogenes. Seborrhoeic dermatitis. aureus or occasionally S. Clinical features Otitis externa may be confined to the meatus (localized) or involve other areas of skin (generalized). A patient with acute mastoiditis will have a more marked post-auricular swelling which may be fluctuant. and herpetic infection. Careful examination will usually distinguish furunculosis (common) from acute mastoiditis (now much less common). Neurodermatitis. Otalgia occurs with furunculosis. Symptoms of infection elsewhere in the head and neck. diffuse otitis externa and herpes infections. Reactive. swimming habits. In furunculosis this is because post auricular oedema is superimposed on the plate. Keratitis obturans. 2. excess squamous debris suggests chronic eczema or mycosis and hypertrophic meatal skin suggest chronic disease It is not uncommon to find the ear canal occluded by oedema in a patient with acute otalgia. Localized infection can be circumscribed or diffuse while generalized infection can be either primary otological or primarily dermatological. There is no pain on moving the pinna and there will be a preceding history of acute suppurative otitis media. neurodermatitis or mycotic infection. Eczema. severe itching suggests eczema. seborrhoeic dermatitis. displacing the pinna down as well as forwards. Inquiries regarding direct trauma to the ear canal. Exceptionally this node may break down to cause diffuse tenderness and oedema which may displace the pinna slightly forwards and there is always pain on moving the pinna. mycosis or acute trauma. usually by S.

aeruginosa. Swimming is inadvisable and precautions taken when bathing to prevent water entering the ear canal. Its low pH is lethal for many bacteria including pseudomonas. malignancy of the EAM or middle ear and malignant otitis externa. impregnated with 10% ichthammol in glycerine. The ears should be kept scrupulously dry until resolution. and antibiotic/ antimycotic sensitivity. Splinting the meatus. the hygroscopic action of which reduces meatal swelling or a pope’s sponge earwick onto which eardrops containing an antibiotic and steroid mixture are applied. Follow-up and aftercare Treatment should continue for at least one week after resolution because of the tendency to recurrence particularly in otomycosis. 3. The overwhelming symptom is a constant deep otalgia and it may cause 7–12th cranial nerve palsies. The two recommended choices are 12 millimetre ribbon gauze. meningitis. Malignant otitis externa This condition describes an otitis externa which progresses to an osteomyelitis initially of the tympanic plate which then may spread to involve the skull base and petrous portion of the temporal bone. The condition should be suspected in a patient with granulation tissue deep in the external meatus which does not settle with the usual treatment. When such a patient develops a facial nerve palsy the differential diagnosis is between the ASOM (almost always secondary to a dehiscent horizontal portion of the facial nerve). Itchy reactive conditions may benefit from a course of beclomethasone ear drops and an 8% solution of aluminium acetate or acetic acid ear spray is recommended in patients with chronic otitis externa after the acute infection has been eradicated. 8% aluminium acetate ear drops which act as an astringent may be considered. Management 1. Meticulous and regular aural toilet paying particular attention to the anteroinferior meatal recess. and a high definition CT scan of the petrous temporal bone are required to make the diagnosis. Splinting will be necessary when there is EAM oedema preventing an adequate view of the tympanic membrane on otoscopy implying that ear drops will not reach the deeper recesses of the ear canal. sigmoid sinus thrombosis. CSOM. . brain abscess and death. 2. The diagnosis is often not considered until a cranial nerve palsy has developed. In resistant cases. including fungal culture. It is most common after middle age. Histological and microbiological examination of granulation tissue.212 OTOLARYNGOLOGY Investigations A culture swab should be taken for microbiological culture. The dressing should be changed at least every 48 hours until the canal swelling has settled sufficiently to allow any applied drops to reach the anteroinferior recess directly. in diabetics and is usually caused by P. In most reactive conditions the above regime is also recommended in order to prevent secondary infection of a raw ear canal surface.

p. Vol. Further reading Hammond V. 5. p. Opiate analgesia may be required to control the deep otalgia. The dose and duration of treatment is decided after discussion with a senior microbiologist and by monitoring clinical response but often therapy has to be continued for six weeks or more. p. Acute otitis media. 38.OTITIS EXTERNA 213 Treatment Appropriate intravenous antibiotics as gleaned from the culture and sensitivity results should be commenced. Scott-Brown’s Otolaryngology.). In: Booth JB (ed. London: Butterworth. 6th edn. 1997. 3. Chronic otitis media. . Related topics of interest External ear conditions. Diseases of the external ear. Even with aggressive treatment there is still a significant mortality. 89.

grey or an amber yellow colour. There is no difference in effusion rates between those children who have large versus small adenoids. Pathology The prevalence of OME is highest in young children (40% at 2 years) and decreases with age so that it is uncommon in teenagers (1% at 11 years). Sequalae such as retraction pockets and even cholesteatoma may ultimately develop. Attic and posterior retraction . In most cases (90%) spontaneous resolution is the rule. noticed by parents. in boys. The tympanic membrane can look dull red. Learning difficulties and speech delay account for the bulk of the remainder. in those with allergy and in the children of parents who smoke. and recurrent infections and otalgia are uncommon features of this condition (1–2%) although they are common complaints in childhood. It can bulge forward or be retracted.OTITIS MEDIA WITH EFFUSION (GLUE EAR) Aetiology The fundamental pathology is Eustachian tube dysfunction.and mucoproteins and containing inflammatory cells which fill the middleear cleft. This ultimately causes an inflammatory response in the middle-ear mucosa and the production of glue: thick. parental smoking. tenacious mucus rich in glyco. in children with cleft palate or Down’s syndrome. allergy and reduced overall nasopharyngeal dimensions. and not because it mechanically obstructs the orifice of the Eustachian tube. The underlying Eustachian tube dysfunction leads to a chronic reduction in middle-ear pressure. whether persistent or intermittent. but there are associations with recurrent upper respiratory tract infections. relatives or teachers or picked up at routine screening is the presenting symptom in over 80% of cases. The adenoid is recognized as an important contributor to otitis media with effusion (OME) because it is a source of pathological bacteria. punctuated by numerous remissions and relapses. The exact cause for this remains in doubt. Examination may or may not reveal a middle-ear effusion depending on the activity of the process at consultation. The prevalence is also higher in the winter months. Hearing impairment. Clinical features The presence of fluid in the middle-ear cleft leads to a conductive hearing loss of variable severity and is responsible for most of the clinical features. with the more severe cases tending to present earlier. Most cases present between the age of 3 and 6 years. In a small number of persistent and severe cases there is progressive atrophy and retraction of the tympanic membrane. The otoscopic appearance of the effusion varies.

Bawden R. In the more severe cases the insertion of ventilation tubes improves hearing and shortens the overall duration of the condition. Air bubbles or a fluid level can occasionally be seen. Pure tone audiometry if feasible will show a conductive hearing loss. Further reading Maw AR. Impedance audiometry will show a flat tympanogram (type b) which is typical of otitis media with effusion and helps distinguish the disease from Eustachian tube dysfunction and otosclerosis. British Medical Journal. but is significantly less effective than grommets. 306:756–760. Tiwari RS. For many children explanation and reassurance to the parents are all that is required. A sizeable proportion of affected children (25%) will require further subsequent grommet insertion. The benefits of adenoidectomy are greatest between the ages of 4 and 8 years. Grommets extrude after approximately 9–12 months following which some form of review is required to recheck the hearing. The benefits of ventilation tubes may be augmented by combination with adenoidectomy. Investigation An audiogram appropriate to age and impedance audiometry are all that is required. 13: 171–177. There is no good evidence that swimming with unoccluded ears increases the risk of infection. Grommets should be used rather than T-tubes. Medical treatment has little role to play in this condition: antihistamines and decongestants have no useful effects and antibiotics produce short-term improvements. Maw AR. but grommet removal may be required if the condition fails to settle. Infections should be treated by aural toilet and antibiotic/steroid ear drops in the first instance. Tympanosclerosis is associated with multiple episodes of grommet insertion and intratympanic bleeding at myringotomy. 1988. Spontaneous resolution of severe chronic glue ear in children and the effect of adenoidectomy. Children with glue ear: how do they present? Clinical Otolaryngology. The main complications of grommets are infections and the development of tympanosclerosis (which is found in 30– 40% of children 1 year after grommet insertion). A review visit after 3 months is useful to establish the persistent nature of the patient’s condition. . mini-grommets seem to cause less but tend to extrude sooner. Follow-up and aftercare Grommets require little aftercare. in particular a persistent hearing loss. Compliance can also be a problem. but do not affect the long-term course. 1993. Management Management should be appropriate to the severity of the symptoms and should always take account of the natural history of the condition towards spontaneous resolution. but bony erosion is relatively unusual. Tonsillectomy does not seem to influence the condition. which are associated with an unacceptably high rate of residual perforation (up to 50%).OTITIS MEDIA WITH EFFUSION 215 pockets may occur. although some form of ear plug should be worn when shampooing (soap reduces the surface tension of the water). Auto inflation of the Eustachian tube using the Otovent device has been shown to give useful results. tonsillectomy and insertion of ventilation tubes (grommets).

344. . Paediatric hearing assessment. p. 128. 239.216 OTOLARYNGOLOGY Related topics of interest Impedance audiometry. p. p. Tympanosclerosis.

these travelling waves reach maximal amplitude at specific points along the cochlea. The outer hair cells at the region of maximal travelling wave amplitude vibrate in synchrony with the stimulating signal while the OHCs on either side of this region suppress vibration of the basilar membrane. Spontaneous OAEs (SOAEs). The outer hair cells also detect these vibrations but.OTOACOUSTIC EMISSIONS Using modern computing technology and signal averaging techniques. 3. The signal is very different for each individual but remains fairly constant for any given ear. These are recorded at the frequency of a stimulating pure tone. occur in response to short-lasting stimulatory acoustic signals (usually clicks or tone bursts). TEOAEs occur in almost all human ears with . usually between 0. thickness and consequently stiffness of the basilar membrane. They appear to have little clinical or research use. Types of otoacoustic emissions Four classes of OAE exist: 1. These outer hair cell vibrations can be detected in the external auditory meatus as otoacoustic emissions. have a motor function. 2. outer hair cell vibrations can be detected in the external auditory meatus as otoacoustic emissions (OAEs). They were first described by David Kemp in 1978 and represent an objective measure of cochlear function. These are low-level signals which occur without external acoustic stimulation in about 40–50% of the normal hearing population. The inner hair cells are purely sensory and are responsible for detecting these vibrations and producing neural impulses to allow them to be perceived by the central nervous system as sound. Sound vibrations pass from the environment through the external and middle-ear systems to cause vibrations of the cochlear perilymph. Acoustically evoked OAEs are almost never found in ears with a hearing level worse than 40 dB. This mechanism allows the finetuning found in the healthy cochlea. These vibrations produce travelling waves in the basilar membrane. they vary in terms of occurrence and intensity and consequently have little use in clinical monitoring. Physiology The cochlea provides an elegant mechanism for transforming the physical properties of sound into electrical neural impulses. As a result of the gradient of width. These signals. These vibrations are detected as a result of shearing forces on two separate hair cell systems in the organ of Corti: the inner (IHCs) and outer (OHCs) hair cells. High frequencies are represented at the basal turn and low frequencies at the apical portion. Transient evoked OAEs (TEOAEs). Although they are relatively constant in frequency. Stimulus-frequency OAEs. in contrast.7 and 4 kHz.

easy to test and do not require an anaesthetic. . Probst R. 1997. 1992. 78. Clinical uses Although still a research tool for the investigation of cochlear function. Advances in Oto-Rhino-laryngology. but are of greater amplitude and wider frequency range in children. Related topics of interest Evoked response audiometry. 27(2): 71–159.218 OTOLARYNGOLOGY hearing levels better than 40 dB. p. The acoustic stimuli are usually broadband clicks. Unlike a tympanometer. the use of evoked OAEs has now found a place in clinical practice in the screening of neonates and high-risk infants for hearing loss. British Journal of Audiology. Further reading 3rd International symposium on cochlear mechanisms and otoacoustic emissions. Stimulation with two pure tones of specific frequency and intensity ratios gives rise to DPOAEs. OAEs can be demonstrated on either a visual or print-out display. An OAE analyser consists of a mobile probe which contains a sound emitter and microphone for recording. at a maximal rate of 50/s. 239. Evoked OAEs are quick. Harris FP. Distortion-product OAE (DPOAE). by the use of appropriate frequency filters and time window averaging. The sensitivity and specificity of the test is sufficiently good that there are widespread recommendations that all newborn infants are screened for hearing loss by OAE prior to discharge from hospital. These characteristics make them an ideal tool for investigating frequencyspecific cochlear function. an airtight seal is not required. 1993. Otoacoustic emissions. p. The stimulated signals are then received and fed to a signal processor where. Research is still being undertaken into the optimal method of producing and subsequently analysing OAEs. they are finding increasing use for clinical screening and research. 53:182–204. They are nearly always present in normal hearing ears and can be measured in the 6–8 kHz range. 4. OAE measurement. in contrast to electrical evoked response audiometry. Paediatric hearing assessment. As they are relatively quick and easy to measure.

Loss of pinna tissue. Intracranial complications—lateral sinus thrombosis. including degloving injuries. Perichondritis. Serous or a purulent labyrinthitis. • Ossicular chain discontinuity. Inner ear • • • • Perilymph fistula from either a round window rupture or from the oval window. extradural. Otitis externa. meningitis. intracerebral (cerebellar and temporal lobe) abscess or haematoma and otitic hydrocephalus. Occlusion of the external canal by clot. Conditions caused by such trauma are described below. Middle ear • Tympanic membrane haematoma and petechiae. middle or inner ear in isolation or in combination. • Tympanic membrane rupture with or without the deposition of squamous epithelium within the middle ear. • Haemotympanum and acute non-suppurative otitis media. External auditory meatus stenosis. • Facial nerve injury. subdural. External ear • • • • • • Subperichondrial haematoma. • Acute suppurative otitis media. Labyrinthine ‘concussion’. There may be a fracture of the temporal bone and other skull base fractures.OTOLOGICAL ASPECTS OF HEAD INJURY A blow to the side of the head by a blunt or sharp instrument may cause injury to the external. .

2. Longitudinal fractures. Facial nerve injury occurs immediately in half of these fractures. Symptoms of secondary endolymphatic hydrops may be caused by involvement of the vestibular aqueduct in the fracture line. This usually heals without residual conductive deafness if infection is prevented. A haemotympanum and ruptured tympanic membrane will occur if the fracture line extends to the middle ear cleft. In the absence of a facial palsy the ear should be left untouched in the early post injury period. Sequelae are unusual in longitudinal fractures and a conductive hearing loss is unlikely to be due to a traumatic ossicular discontinuity. the only sign will be bruising of the postauricular skin (Battle’s sign).220 OTOLARYNGOLOGY Temporal bone fractures These are classified into longitudinal. Occasionally with a fracture of the squamous temporal bone. It should resolve when the ear canal skin and tympanic membrane heal. In 80% of temporal bone fractures a longitudinal fracture is the dominant fracture and usually arises from a lateral blow to the skull. An isolated longitudinal or transverse fracture is unusual. In a pure transverse fracture there is a haemotympanum but no bleeding from the ear because the tympanic membrane remains intact. Over 80% of temporal bone fractures involve a combination of both longitudinal and transverse fractures. nystagmus to the opposite ear. A sensorineural hearing loss is usually secondary to inner ear concussion and therefore temporary. These fractures occur with a more severe head injury so otological symptoms may not become apparent until recovery from the acute head injury. The fracture extends from the squamous temporal bone in the roof of the bony external auditory meatus to the tympanic membrane and the roof of the middle ear before turning anterior to the labyrinth where it may involve the carotid canal. a type of longitudinal fracture. raised intracranial pressure and focal neurological signs. Management The general management of the head injury takes precedence but it is important to avoid introducing infection into the ear so prophylactic antibiotics are often indicated. Labyrinthine capsule disruption causes an irreversible sensory hearing loss. Facial nerve injuries are uncommon although CSF otorrhoea is more common with this fracture. This is the dominant fracture in 20% of temporal bone fractures and usually arises from a blow to the front or back of the skull. 1. The latter is suspected when an initial serosanguinous aural discharge becomes clear. usually a dead ear. IXth to XIIth cranial nerve injury. Transverse fractures. Temporal bone fractures often have a mixed longitudinal and transverse component and this will be suspected from combined clinical features. Clinical features Longitudinal fractures tear the skin of the external auditory meatus and tympanic membrane to cause swelling of the canal skin and bleeding from the ear. . depending on the orientation of the fracture line to the long axis of the petrous temporal bone. severe vertigo. These findings should be presumed to indicate such a fracture following a head injury. The fracture extends across the long axis of the petrous bone through the labyrinthine capsule and is demonstrated with plain temporal bone radiographs in 50% of cases. transverse and mixed.

Related topics of interest Facial nerve palsy. usually from the middle fossa and allow exploration by an otoneurosurgeon. A high definition CT scan of the temporal bone on bone setting with fine (1 mm) cuts is required. a bony spicule may be impinging on the nerve or there may be complete transection of the nerve). If there is a fracture in the tympanomastoid segment. Others argue that a high quality scan is unlikely to miss a fracture and that exploring the nerve in such circumstances may further traumatize the nerve. If such a patient is seen soon after the injury and there is a clear history of an immediate and total lower motor neurone facial palsy. 244. this suggests a severe injury to the nerve (it may be caught in a fracture line or be compressed by a fracture. Even if there was no fracture then a neuropraxia or axonotmesis may have occurred and early decompression may prevent further injury to the nerve. CSF otorrhoea is confirmed by the presence of glucose and 2 transferrin. 1992. Perilymph fistula. p. Should the leak persist a CT scan using intrathecal metrisamide may identify the site of the leak. many otoneurosurgeons would advocate a complete decompression of the nerve from the internal auditory meatus to the stylomastoid foraman. 13:552–555. the injury is likely to be secondary to a neuropraxia and a conservative policy should be adopted. with about 90% recovery to House and Brackmann grade I or II. The scan may have missed a bone splinter impinging on the nerve and waiting at least 14 days for nerve conduction studies may result in irreparable damage to the nerve. It therefore follows that an otoneurosurgeon should be contacted if decompression of the nerve is contemplated. The decision therefore depends on the surgeon’s experience and expertise. American Journal of Otolaryngology. Kelly RH et al. . In patients who develop a facial palsy hours or days after injury or in whom the palsy is partial. Hirsch BE. If no fracture is seen on a CT scan many otoneurosurgeons would still advocate complete decompression of the nerve from the IAM to the stylomastoid foraman.OTOLOGICAL ASPECTS OF HEAD INJURY 221 Management of a facial palsy following a head injury It is unusual for otolaryngologists to see a patient with a significant head injury soon after the injury as they will have been managed by neurosurgeons. A policy of bed rest but sitting up to reduce intracranial CSF pressure and antibiotic cover to prevent intracranial infection usually allows resolution to occur after about ten days. Traumatic perilymph fistula is discussed elsewhere. The latter segment is important as it is in this region where the bony canal is narrowest and the nerve most susceptible to injury from oedema. decompression of the horizontal and labyrinthine segments of the nerve and this requires otoneurosurgical input. p. If it is less than 10% after 14 days then the consensus view is to explore the nerve. Electromyography will provide an indication of the severity of the injury and the prognosis in those patients where the history is not clear. If the summating potential is more than 10% of normal after 14 days the prognosis is good. No matter what the finding of the scan such a case should be discussed with an expert otoneurosurgeon. A fracture of the labyrinthine segment requires. decompressing the tympanomastoid segment and the labyrinthine segment. as a minimum. 2 transferrin application in otology. 92. Further reading Bassiouny M.

Blood stained discharge is also a feature of carcinoma of the middle ear. it is wise to consider a carcinoma. CSF rarely discharges from the ears spontaneously but may do so following skull base surgery or more commonly trauma. blood (acute otitis media. Cerebrospinal fluid. trauma. if there is a mucoid component to the discharge it usually arises from the middle ear via a perforation of the tympanic membrane. 3.OTORRHOEA Definition Otorrhoea is the discharge of material from the external auditory meatus. There are no mucinous glands in the external canal. This combination generally leads to soggy white debris collecting in the canal and a thin white watery discharge from the ear. Clinical features The character of the discharge depends on (and therefore gives clues to) its source. 2. debris. In addition. 1. Acute inflammatory conditions of the external meatus therefore tend to produce a watery. Other causes include: wax. pain and tenderness. in addition to the discharge. which may lead to bleeding from the ear. The middle-ear cleft is well endowed with mucous glands. The cardinal symptom of otitis externa is itchiness. The external canal may also be the subject of trauma. In both cases the fluid may initially be mixed with blood and may be recognized by the halo sign in which there is a clear ring of moisture surrounding the blood after absorption on to blotting paper. when it will develop in about 5% of cases. if a cholesteatoma should become infected the discharge tends to be particularly unpleasant and once smelt is never forgotten. Chronic otitis media is not typically characterized by pain. A serosanguinous discharge is common with chronic otitis media when the middle-ear mucosa has become granular and polypoid. there is glandular hyperplasia and there may be blood as the mucosa bleeds easily. Trapped keratin is offensive. Thus. and CSF (usually following a fracture). It is both a symptom and a sign. they tend to provoke a hyperkeratosis. It is not a diagnosis. This is due to the faster diffusion of . so in patients where chronic otorrhoea becomes painful and fails to respond to the usual conservative measures. serous exudate or transudate. External ear. Middle ear. Causes Otitis externa and active suppurative otitis media are the commonest diseases causing this problem. neoplasm).

If the tympanic membrane is intact CSF may still leak from the ear should there be a fracture in the roof of the ear canal. This will invariably require attention to the primary or secondary otitis externa by thorough aural toilet and possibly the insertion of a wick. p. Further reading Applebaum EL. St. Chronic suppurative otitis media. A swab should be taken for culture and sensitivity (bacteria/fungi). Any granulation type tissue removed should be sent for histology. CSF leaks. p. diagnosis of cause. Head and Neck Surgery.OTORRHOEA 223 the less viscous CSF. This may not be possible at the initial consultation owing to swelling and debris in the external auditory meatus. Conservative management includes sitting upright in bed and avoidance of manoeuvres that raise intracranial pressure (e. 965–974. Otitis externa. 1. coughing. The mainstay of therapy is aural toilet. p. p. 209. conservative management is reasonable for the first few postoperative days but surgical repair will be required if the leak fails to settle. This enables a thorough assessment. Otolaryngology. Chow JM. 1993. straining). . Otherwise it may pass down the Eustachian tube and become evident as rhinorrhoea or post-nasal drip. Cholesteatoma. Post-traumatic leaks usually resolve spontaneously within a short period. for instance. Fluorescein injected by lumbar puncture may be helpful in finding the site of the leak at the time of surgery. Treatment will often commence on the basis of a best guess diagnosis. Management Optimum management depends on making an accurate diagnosis. Related topics of interest Acute suppurative otitis media. vol. 5. Treatment of the otitis externa will be sufficient if this is the diagnosis. Although the history will give many clues. 35. but surgical repair will be required if they continue beyond 14 days. latrogenic leaks should hopefully be recognized and repaired at the time of surgery. Middle-ear disease will demand treatment on its own merits. and allows better penetration of any topical treatments.g. Prior to any surgical exploration a thorough radiological assessment of the temporal bone should be undertaken to try to establish the site of the leak. the diagnosis is usually not made until the tympanic membrane has been visualized. Otological aspects of head injury. ideally by microsuction clearance. Differentiation of CSF from thin serous discharge from a middle-ear cavity may be more difficult but can be done by estimation of the glucose content or by confirming the presence of 2transferrin in CSF. If this is not the case. (eds). At the time of definitive diagnosis more appropriate treatment can be continued. In: Cummings CW et al. This is especially important in patients who have already been on treatments which have not worked. Louis: Mosby. 38. 2nd edn. p. This is best achieved with highresolution CT scanning and the subarachnoid injection of Omnopaque 500. The type and method of repair employed will depend on the site and cause of the leak and to some extent the state of the middle ear and the patient’s hearing. Patients with CSF otorrhoea should be initially covered with prophylactic antibiotics to reduce the risk of meningitis. it would be inappropriate to obliterate the middle ear of an individual with normal hearing. 218.

The incidence of otosclerosis is higher. but not all consultants perform stapedectomy. but will nowhere near approach the 1% incidence that is often quoted in major texts. the base of the styloid process. The average consultant/trainee team in the UK perform on average eight stapedectomies per year (range 0–30). It is uncertain whether cochleovestibular symptoms arise directly from this encroachment or from factors released by the plaque or from both.5–2% of the population (the prevalence) and the subclinical disease affects about 10% of the population. . Prevalence and incidence The clinical disease has been estimated to effect 0. 2. It is an expression of a genetic mutation in collagen metabolism which is only phenotypically expressed in bone derived from the otic capsule. It is an expression of humoral autoimmunity to type II collagen. The incidence of stapedectomy. Eighty-five per cent of otosclerotics have bilateral disease. perhaps 0. Symptoms occur when these foci fix the stapedial footplate and encroach upon the labyrinth. the semicircular canals. Foci have also been noted in the region of the fissula post fenestram. the petrosquamous suture and in the cochlea. the round window. even if we were to assume every consultant performed eight stapedectomies per year. The incidence of clinical disease (number of new cases per year) is much lower.0067%.05% as we would not expect all subjects with clinical otosclerosis to have a stapedectomy. lacunae.OTOSCLEROSIS Definition Otosclerosis is an autosomal dominant disease of incomplete penetrance affecting bone derived from the otic capsule in which mature lamellar bone is replaced by woven bone of greater cellularity and vascularity featuring large Haversian canals. It is an expression of persistent measles virus infection of otic capsule-derived bone. would be approximately 4000 per 60 million or 0. canaliculi and marrow spaces. The three main theories of pathogenesis are: 1. 3. Pathogenesis Otosclerotic foci are most commonly located just anterior to the oval window in the region of the fissula ante fenestram.

The masked bone conduction curve typically shows a dip at 2000 Hz which may be small or exaggerated particularly when there is only a slight cochlear loss (Carhart’s notch). Vertigo. Present in 75% of patients especially when there is a cochlear element to the deafness. Crural atrophy. Noticed in most cases before the age of thirty. Deafness. Sodium fluoride.OTOSCLEROSIS 225 Otosclerosis is more common in Caucasians. a pink tinge of the tympanic membrane imparted from dilated blood vessels on the mucous membrane of the promontory. Its use remains controversial. Unreliable as a diagnostic aid although it may be useful in selecting the more suitable ear for surgery in bilateral otosclerosis with a symmetrical PTA by suggesting the more rigid stapes. Better hearing in noisy surroundings is often described—paracusis Willisi. 2. Paget’s disease (usually produces a mixed hearing loss). Management 1. Osteogenesis imperfecta. Investigations 1. Congenital cholesteatoma. Differential diagnosis • • • • • • • • Fibro-osseous foot plate fixation. Symptoms may mimic benign paroxysmal positional vertigo. and on the cochlear reserve. Rinne’s test usually suggests a conductive hearing loss. . The Weber may be referred to either ear depending on whether disease is unilateral or bilateral. The curve shows a predominately high tone loss when there is severe cochlear impairment. Mild and usually transient. Ossicular discontinuity. 2. Tinnitus. Speech audiometry. With amplification the score approaches one hundred with normal cochlear function but the score falls according to the severity of the cochlear loss. Clinical features The main symptoms are: 1. Ten per cent of ears display Schwartze’s sign. No major randomized prospective double blind trial has been performed to assess its effectiveness. menstruation and the menopause may cause the disease to progress rapidly. 2. 3. A hearing aid. Congenital foot plate fixation. perhaps because women are more likely to seek advice because pregnancy. Fixed malleous-incus syndrome. It causes no other otoscopic signs. Impedance audiometry. In addition to a conductive hearing loss there may be cochlear impairment. Masked air conduction typically shows a loss which is greater at low frequencies when there is minimal cochlear impairment but the frequency response curve flattens and then shows a predominantly high frequency loss as cochlear impairment progresses. Pure tone audiometry (PTA). 3. Women are more likely to have bilateral clinical disease. A female: male ratio of 2:1 has been noted.

A 0.226 OTOLARYNGOLOGY 3. The Causse technique comprises a 0. Large fenestra. • Open the mouth on coughing or sneezing.6 mm fenestra drill piece and 0. The incidence reported by expert otologists varies from less than 1–4% and a further 10% may have no better or worse hearing than pre-operatively.4 mm prosthesis. Complications of stapedectomy 1. 2. . • There is a very small chance that the facial nerve will run an anomalous course either splitting around or coursing inferior to the oval window and may be injured. The otologist aims to get complete or over-closure of the air bone gap. Preoperative counselling • A hearing aid is an alternative method of treatment. a stapedotomy needle. The smaller the fenestra. or an argon or KTP laser is used to create the fenestra in the stapes footplate. Chorda injury. Overhanging facial nerve. • • • • • Tympanic membrane tear. Persistent stapedial artery. Stapedectomy. Peroperative. If both ears are suitable for surgery in bilateral disease the poorer hearing ear should be chosen. A micro drill. Tympanosclerosis arthrodesing the incudostapedial joint. Over-closure is possible because of the Carhart effect and is greatest at 2000 Hz (see audiometry chapter). The minimum requirements are at least a 15 dB conductive hearing loss with 60% speech discrimination. the smaller the risk of a high tone cochlear hearing loss. The ear including the external ear canal should be dry. It is contraindicated in pregnancy. 8 mm fenestra over which a vein graft is placed and a 0. • Taste may alter or be lost on one side of the tongue (damage to chorda tympani). • Vertigo may be present immediately postoperatively and in a minority there may be a permanent sense of imbalance. Technique 1. • Tinnitus may not improve and may be more intense after surgery. Second ear stapedectomy is still controversial but is advocated by many who perform the small fenestra procedure.4 mm prosthesis are popular. A portion of the footplate is removed with picks and fine right angle hooks. Postoperative advice • Avoid diving when swimming. Small fenestra. lifting heavy objects and aggressive nose blowing. An attempt is usually made to seal the oval window with a vein or fat graft prior to prosthesis insertion. • A dead ear may occur with stapedectomy. • Avoid flying for the first three weeks post-operatively.

Revision stapedectomy There are three main groups who should be considered for revision stapedectomy: (a) Patients who have redeveloped a conductive hearing loss after stapedectomy. . A high definition CT scan may detect an otosclerotic plaque. An immediate dead ear may arise from the footplate problems noted above. Cochlear otosclerosis Consider when there is a family history of otosclerosis and progressive sensorineural hearing loss in early adult life of no apparent cause. This lies as close as 0. Injury to the saccule. It may be the cause of a dead ear from an apparently uncomplicated procedure. • Late detachment or displacement of the prosthesis. Late. Floating footplate. Early. (c) If vertigo persists or develops several weeks after stapedectomy. a prosthesis which is too short or a dislocated malleo-incudal joint. Persisting primary perilymph fistula. An immediate dead ear may occur if too long a prosthesis injures the saccule. Loose attachment of incus and prosthesis. or erosion of the long process of the incus due to pressure necrosis from the loop of the prosthesis. • Secondary perilymph fistula. The commonest causes are a dislocated prosthesis (from either the oval window or from the incus). Displacement of prosthesis from oval window. Look for Schwartze’s sign on otoscopy. Footplate granuloma.OTOSCLEROSIS 227 • • • • Perilymph flooding.4 mm beneath the footplate. 3. It is easily disturbed when performing the stapedotomy or inserting the prosthesis. (b) Patients who have had no closure of the air-bone gap following stapedectomy. This is due to too long a prosthesis irritating the saccule. but is usually 1–2 mm beneath. probably because of injury to the saccule with each of these events. particularly if associated with loud noises or with applying pressure to the external ear canal. The commonest causes of a persistent conductive hearing loss are a dislocated prosthesis. • • • • • Detachment of prosthesis from incus. Depressed footplate. 2. • Necrosis of the long process of the incus.

Incesulu A. A review of 308 cases of revision stapedectomy. Revision stapedectomy: intraoperative findings. Related topics of interest Labyrinthitis. HNO. 1998. Further reading Altermatt HJ. 107:1185–1192. 108: 1794–1800.228 OTOLARYNGOLOGY The overall results of revision surgery are not as good as primary surgery. results and review of the literature. Han WW. 244. . Fishman A. 1992. Gerber HA. McKenna MJ et al. 301. Gaeng D et al. Immunohistochemical findings in otosclerotic lesions. Hammerschlag PE. Laryngoscope. Reported post-operative sensorineural loss in a number of series varies from 0. 40: 476–479. p.7 to 20%. Speech audiometry. p. 134. p. Laryngoscope. Scheer AA. Perilymph fistula. 1997.

Geneticists have found that susceptibility to aminoglycoside ototoxicity is transmitted exclusively by women. the latter the number of free methylamine groups (-NHCH3). particularly at the basal turn of the cochlea and to spiral ganglion neurons occurs with cochleotoxicity. Findings in animals suggest an elimination half-life of 6 months within the outer hair cells. cochlea or the vestibulocochlear nerve. The concentration in the endolymph therefore depends on the ratio of secretion to resorption which in turn depends on the drug’s serum concentration. This in turn causes a reduction in intracellular adenosine triphosphate (ATP) production with a resultant toxic accumulation of ions such as calcium and potassium within the cytoplasm and ultimately cell death. Aminoglycosides All aminoglycoside antibiotics have a tendency to be predominantly either cochleotoxic (e. commonly therapeutic agents. the ampullary cristae and the maculae of the saccule and utricle. There are over 200 ototoxic substances but only a small group of drugs in common therapeutic use are regularly associated with ototoxicity. This may explain the cumulative ototoxic effects of aminoglycosides and why some patients develop ototoxicity only after a prolonged course or repeated courses of aminoglycosides. .OTOTOXICITY Ototoxicity is the partial or total reduction in cochleovestibular function caused by the interaction of chemicals. Mitochondrial DNA is inherited maternally because the tiny amount of cytoplasm in spermatozoa cannot transmit mitochondrial DNA.g. Electron microscopy confirms that injury to the first row of the outer hair cells. gentamicin and tobramycin). Mechanism of action Current opinion holds that secretion of aminoglycoside from the stria vascularis into the endolymph and perhaps from the vessels of the spiral ligament into the perilymph occurs with active uptake of antibiotic from the perilymph into the endolymph. neomycin and kanamycin) or vestibulotoxic (e. It is not X-linked but can be explained by mitochondrial inheritance. It is important to note the damage to the vestibular and cochlea sensory cells is greatly enhanced by the synchronous use of a loop diuretic.g. Light microscopy shows destruction of the sensory cells of the organ of Corti. Aminoglycosides cause mitochondrial dysfunction in susceptible patients so that there is inhibition of translation or mistranslation of mitochondrial protein synthesis. with the vestibule. The former relates to the number of free amino groups (-NH2). Resorption by the stria clears the endolymph of aminoglycoside.

Loop diuretics Frusemide. Aminoglycosides are excreted by the kidney and the administered dose must be reduced in renal failure. Since 5% of this group become deaf purely as a result of their disease the contribution of the diuretic to the deafness is. It is of note that two iron chelators. Gentamicin in the presence of iron salts produces peroxidation of arachidonic acid in vitro so aminoglycoside ototoxicity may be caused by free radical formation in the presence of iron salts. in many cases.230 OTOLARYNGOLOGY Studies with preloading antioxidants (in particular glutathione and vitamin C) prior to aminoglycoside exposure have shown a significant protective effect. Withdrawing therapy may prevent further significant deterioration provided renal function is adequate. bumetamide and ethacrynic acid in high doses may produce a reversible high tone sensorineural hearing loss. 2. Light microscopy shows the stria vascularis to be grossly oedematous but the organ of Corti remains essentially normal. Nystagmus may not be demonstrable but caloric testing shows a bilateral decline in labyrinthine function. 3. uncertain.3dihydroxybenzoate reduce gentamicin ototoxicity in guinea pigs in vivo and iron chelators may have a clinical role to play in reducing aminoglycoside ototoxicity in the future. The mechanism is thought to be that antioxidants prevent aminoglycosides being converted enzymatically within the cell to a cytotoxin that causes mitochondrial dysfunction. Neurotrophins such as brain-derived neurotrophic factor protect the spiral ganglion neurons but do not prevent outer hair cell degeneration. presenting some days into treatment and is usually progressive. Preloading with glutathione and vitamin C may become standard practice to minimize ototoxicity. Hypoproteinaemia also increases the chances of cytotoxicity but this can be overcome by administering large doses of glutathione with vitamin C. Vertigo is characteristically a bobbing oscillopsia whereby distant objects appear to jump about on head movement. a large total dose (in gentamicin’s case >1 g) and a subject aged over 60 all increase the chances of ototoxicity. Tinnitus may occur during or after withdrawing treatment. Clinical features 1. It and nitrogen mustard have a similar cochleotoxic effect to the aminoglycosides in causing greatest injury to the first row of outer hair cells particularly at the basal turn of the cochlea but inner hair . Cytotoxic agents Cisplatin is the most important drug in this group as for many it is the drug of choice in palliating head and neck cancer. A pyrexia. Hearing loss is principally high frequency and sensorineural. desferoxamine and 2. A permanent hearing loss is unusual but has been described in renal dialysis and transplant patients. Investigations Monitoring of patients taking these antibiotics by regular inquiring of otological symptoms and by the regular measurement of serum peak and trough levels are necessary to reduce the incidence of ototoxicity and to allow early withdrawal of therapy should they arise. It may become more intense and persistent in spite of drug withdrawal.

Vestibulosedative medication and rehabilitation exercises. As most of the drug is bound to plasma proteins. Aftercare and follow-up Cochleotoxic symptoms require regular pure tone audiometric monitoring until thresholds are stable or improve (temporary threshold shift) in order to quantify the disability. This is usually reversible on withdrawing the drug. In vivo studies in humans have suggested that preloading with diethyldithiocarbamate and an agent known only as WR2721 prior to cisplatin delivery significantly reduces not only ototoxicity but also toxic effects on the gastrointestinal tract. Quinine Formerly used in the treatment of malaria and still used today to control night leg cramps. quinine has cochleotoxic effects similar to aspirin except hearing loss may progress after withdrawing therapy and is more likely to be permanent. hypersensitivity occurs whereby cochleotoxicity develops at therapeutic plasma levels. In a minority. . Salicylates Aspirin in overdose may induce tinnitus and a flat pure tone hearing loss of up to 60 dB.g. Aspirin is cleared rapidly by the kidney so that treatment comprises adequate hydration and the use of an H2 antagonist e. plasmaphoresis is an effective therapy in massive overdose. minimize morbidity and may aid symptomatic recovery by accelerating compensation. e. In those where phenytoin must be used to control the disorder careful monitoring of the serum levels are necessary.and post-dose audiometry is necessary to monitor cochleotoxicity which may be partially reversible on withdrawal of treatment. bone marrow and kidney.g.g. Beta blockers A mixed deafness has been described. the conductive element being secondary to a middle ear effusion. Cooksey-Cawthorne exercises. and degeneration of the stria vascularis. Ongoing studies are taking place to confirm this and also to demonstrate whether the agent affects the tumouricidal effects of cisplatin.OTOTOXICITY 231 cells are also injured. Vestibulotoxic recovery can be symptomatically monitored by out-patient assessment and if necessary quantified by ENG caloric measurements. Anticonvulsants Vestibulotoxicity has been described with phenytoin and ethosuximide. The cochleotoxic effects are generally mild and reversible. omeprazole to prevent upper GI complications. cimetidine or a proton pump inhibitor e. Pre. particularly towards the apex. There is degeneration of spiral ganglion neurons. These ototoxic effects are potentiated by hypoproteinaemia and anaemia. The vertigo may be either acute and reversible on withdrawing treatment or more commonly chronic. The vestibular apparatus is undisturbed and recent work has suggested a direct effect of salicylates on the outer hair cells of the cochlea. The pathogenesis of both the cochleotoxicity and the effusion is unknown.

McLaren J. Variable efficacy of radical scavengers and iron chelators to attenuate gentamicin ototoxicity in guinea pigs in vivo. Mechanism of protection by diethyldithiocarbamate against cisplatin ototoxicity: antioxidant system. 86:15–24. 1995. Related topics of interest Sudden hearing loss. 26:293–300. Hearing Research.232 OTOLARYNGOLOGY Further reading Rybak LP. p. . 1996. Caloric tests. 94:87–93. Hearing Research. 1995. p. Glutathione protection against gentamicin ototoxicity depends on nutritional status. Schacht J. Ravi R. Lautermann J. 346. p. 327. 314. 27. Song B. Vertigo. p. Fundamentals of Applied Toxicology. Somani S. Schacht J. Tinnitus.

It may be expiratory or inspiratory. Bilateral choanal atresia can cause such symptoms but there are other more serious problems in this condition and surgical relief is provided as a matter of urgency. and individual conditions are best discussed through these symptoms. Subglottic stenosis. enlarged adenoids (or tonsils). Problems will nearly always produce noisy breathing (stridor/stertor) or affect the voice (hoarseness). Children with Down’s syndrome and . There are many diseases which can cause paediatric airway problems. webs. is known as wheezing and is the result of an asthma-like condition. A laryngeal lesion is usually characterized by inspiratory stridor and a tracheal lesion by expiratory stridor. Wheezing is the province of the respiratory physician and will not be discussed here. Laryngomalacia. but this topic confines itself to the following conditions: • • • • • • Laryngotracheobronchitis. Any factor which reduces the size of the lumen will therefore have a greater effect in the neonate and child. Noise from the neck region is known as stridor and is caused by narrowing of the respiratory lumen in the upper trachea or larynx. Vocal fold paralysis. the neck or the mouth and nose. Miscellaneous conditions (papillomata. Stridor Abnormal noise during breathing may emanate from the chest. rhinitis and muscular incoordination can all be responsible and each condition should be treated on its merits. Stertor Stertor is noise originating from the back of the mouth or nose. Noisy breathing from the chest is usually expiratory. gastro-oesophageal reflux). Vascular ring. although if high in the trachea it may be ‘biphasic’. cysts.PAEDIATRIC AIRWAY PROBLEMS Introduction Paediatric airway problems are different from adult problems because congenital abnormalities manifest themselves early in life and the airway is significantly narrower. Choanal stenosis.

Tracheostomy is virtually unknown for laryngomalacia and. Epiglottitis produces more severe symptoms which are discussed elsewhere. an associated vocal cord palsy should be suspected and excluded. It is temporary in laryngitis and is the presenting symptom with papillomata. becomes necessary. If further deterioration occurs. The usual finding is a relatively narrow subglottis which will widen with growth. it is self-evident that those who have a small glottis initially will be more affected. intubation is carried out. The commonest cause of persistent hoarseness is the presence of vocal nodules. particularly in the subglottic area. The insertion of a nasopharyngeal tube which projects just beyond the soft palate is helpful in most refractory cases. Laryngo-tracheo-bronchitis This is a very common cause of stridor. This is best done by a paediatric intensivist or anaesthetist and as small a tube as possible is used. The symptoms gradually improve with time but may take several years to stop. The child is closely observed after treatment with humidity. On those unusual occasions when extubation is not possible a tracheostomy will be necessary. Allergic oedema produces similar symptoms. It is due to an indrawing of floppy supraglottic structures (particularly the arytenoids and aryepiglottic folds) during inspiration. dexamethasone and sometimes an adrenaline nebulizer. if considered. a direct laryngoscopy is carried out.234 OTOLARYNGOLOGY cerebral palsy are particularly prone to trouble. Since the diameter of the subglottis in the normal population follows a normal distribution curve. It is characterized by an intermittent stridulous squeak of varying severity. and most of the milder cases will not reach the hospital. As the condition improves a leak appears around the tube and the child is extubated. but they do respond to speech therapy. Infective oedema will narrow the lumen. It may only be slight and present in certain positions. if symptoms are marked. Unilateral vocal cord palsy can also produce a weak or hoarse voice and is seen following cardiac operations. Removal with the laser is only indicated when they are large. antibiotics. where the airway in the child is narrowest and the submucosal tissue lax. The inspiratory stridor accompanied by a harsh cough will usually follow a throat infection. admission to hospital. oxygen. but at worst there would be recession of the chest and suprasternal region and interference with feeding. If the symptoms get worse. preferably to an intensive therapy unit. Laryngomalacia This condition may appear within an hour or two of birth and is the commonest cause of stridor in infants. The diagnosis is confirmed and. nothing need to be done apart from a 3-monthly follow-up with advice to return in the interim if symptoms worsen. and many patients can be treated at home with antibiotics and humidity in the form of steam. . the surplus lax mucosa can be excised from the superior border of the aryepiglottic fold under the microscope or a laser aryepiglottoplasty can be performed. The condition follows a self-limiting course. If severe or if there is parental anxiety. If slight and parental anxiety is absent. Hoarseness Hoarseness indicates an abnormality of the vocal cord. Endoscopy should be avoided in the acute period (as it increases oedema) but should be done to identify an underlying abnormality if attacks recur. These are unlikely to be caused by misuse of the voice as they have been described in the neonate. and they appear more quickly and clear equally rapidly.

The diagnosis is made by laryngoscopy and it is sometimes possible to see the larynx in the awake patient with a transnasal fibreoptic endoscope. More severe cases will require an anterior and posterior split. The baby should be seen at regular intervals and the movement reassessed every 6 months. a tracheostomy becomes necessary. and any additional narrowing due to oedema or scar tissue will tend to cause stridor. although a significant number have other abnormalities. It is useful to reach a consensus by inviting the anaesthetist and any available surgeon present to make an assessment as there is a considerable subjective element. A stent is usually introduced for a few weeks. the child can be left until there is an adequate airway and then decannulated. known as laryngotracheoplasty. The cry is usually normal as adduction is not affected. The parents will require support and must have easy access to the hospital if they are worried. Splitting of the cricoid and upper trachea with insertion of costal cartilage into the split is the standard surgical approach. A large tube predisposes to stenosis. however. but a constitutional tendency to fibrosis is the only explanation for those who develop stenosis after only 2 or 3 days of small tube intubation. An attempt should be made to treat the condition conservatively. wide abduction of the cords must be seen. follow trauma. In some cases the stridor is so bad and indrawing so severe that tracheostomy is the only treatment. Subglottic stenosis The subglottis is the narrowest portion of the paediatric airway. but this is not mandatory. sometimes a progressive stridor develops weeks or months after extubation.PAEDIATRIC AIRWAY PROBLEMS 235 Vocal cord paralysis A unilateral vocal cord paralysis will usually produce no symptoms apart from some weakness of the voice. the cricoid can be split in the neonate and a temporary stent inserted. may need to be repeated before an adequate airway and decannulation is achieved. This operation. The stridor of laryngo-tracheitis is due to temporary oedematous stenosis and a relatively small cricoid ring may first manifest itself with these symptoms. although this is best left until the age of 2 years. It may be impossible to extubate the infant. Decannualation should occur as soon as normal function returns. If the lumen is obviously enlarging. More often. but a bilateral vocal cord paralysis produces a stridor which is very similar to that found with laryngomalacia. as most will recover within 2–3 years. however. In order to exclude the diagnosis. Adduction and passive movements of the cords with respiration can easily be mistaken for normal function and there are occasions when a diagnosis cannot be made with certainty. If there is total stenosis or if a pin-hole lumen persists. The decision to treat the vocal cord surgically should be left for several years and should be made only after thorough and informed consultation with the child and parents. In many cases the cause is unknown. If extubation is impossible. The most severe cases. . but an anterior split will suffice in milder cases. and in the neonate prolonged intubation associated with prematurity is the usual cause. More commonly it is necessary to perform direct laryngoscopy with the baby anaesthetized but maintaining vocal cord function. The size of the subglottis is then assessed under general anaesthesia every few months by passing endotracheal tubes until a snug fit is obtained. surgery is necessary. However. with vocal cord paralysis the symptoms and signs become worse with time as the baby makes stronger inspiratory effort.

5. Larger webs may be opened with the laser. 3. Related topics of interest Epiglottitis. but the laser has made early removal possible. reflux oesophagitis needs to be excluded by investigation. Micrognathia or a large tongue can narrow the upper airway. There is little to be gained from consideration of the vascular abnormalities as these are complex and often confusing to the chest surgeons themselves. 138. Reflux has been implicated in the cause and exacerbation of laryngo-tracheal stenosis and if there is evidence that effective management of reflux improves the primary pathology of even laryngeal papillomatosis. Every neonate with no obvious cause for the stridor should therefore have a barium swallow. Hoarseness and airway problems occur as a result of scarring and can require reconstructive surgery. They usually disappear when immunity develops. . 237. Gastro-oesophageal reflux is widely accepted as an important factor in all sorts of paediatric airway problems. 2. but even a tracheostomy is considered in the worse cases. Laryngeal webs may be congenital or acquired. but in the interim laser removal is required and certain individuals do not develop immunity. 70. Laryngeal carcinoma. Cysts. As many as 80% of laryngomalacia babies are said to have reflux and it is suggested that these be treated empirically with antireflux medication. If they are small and only produce minimal symptoms they are best left alone. p. 1. Where there is no obvious anatomical cause for stridor. Papillomata are viral warts which vary greatly in virulence. Subglottic haemangioma is the most common neoplasm of the infant airway. Even after correction there may still be narrowing due to tracheomalacia. haemangiomata and lymphangiomata can occur in the subglottis and less often in the glottis and supraglottis. Endoscopy will show a pulsatile narrowing of the trachea and correction is carried out by the chest surgeons. 336. A conservative approach can often be taken as many lesions involute as the infant grows. as in the Pierre-Robin syndrome. but reconstructive surgery with stenting can be necessary. 4. Stridor and stertor. which is believed to be caused by softening of the tracheal rings by the pulsatile vessel. Paediatric endoscopy. Cysts can also be aspirated and sometimes removed. p.236 OTOLARYNGOLOGY Vascular ring Abnormal blood vessels in the chest may compress the trachea and oesophagus and classically produce an inspiratory and expiratory stridor associated with feeding difficulties. Nursing in the prone position is helpful. p. 311. a tracheostomy may become necessary. Miscellaneous Numerous lesions in the laryngeal region will encroach upon the airway and cause stridor. p. which will demonstrate the oesophageal narrowing. p. If very virulent and florid. Tracheostomy.

the hypopharynx. Essentially. Laryngomalacia is easily distinguished by the indrawing of the arytenoids. When a tracheoscopy or bronchoscopy is also to be performed. paediatric endoscopy involves the use of a rigid laryngoscope or bronchoscope (with a telescope incorporated). For the purpose of identifying a lesion in the glottis or subglottis. postnasal space and larynx can be done in the child or infant. oropharynx and mouth are examined with . Laryngoscopy Adult laryngoscopes such as the Kleinsasser range can be safely used for children.PAEDIATRIC ENDOSCOPY Endoscopy of the respiratory tract is commonly carried out by the otolaryngologist. the tip of the laryngoscope is passed posteriorly to the epiglottis as this structure may obstruct the view. physician or anaesthetist. In most cases. Subglottic stenosis is identified on laryngoscopy if the vocal cords are not in spasm. Where a full examination of the respiratory tract is required. An endotracheal tube is in place for the induction of anaesthesia. but normal vocal cord movement is more difficult to identify. the tip of the laryngoscope is best placed in the vallecula to avoid fixation of the glottic and supraglottic structures. If vocal cord movement or laryngomalacia is being assessed. although subsequent treatment is often the province of the chest surgeon. clinical record and follow-up comparisons. Endoscopy is best avoided within a week following infection and oedema should first be allowed to subside. The fibreoptic endoscope can be passed through the nose or through a laryngeal mask and the latter procedure is very useful in the diagnosis of vocal cord paralysis. it is best to watch glottic and supraglottic movement at the end of the procedure while the patient is regaining consciousness and producing more movement. Paediatric oesophagoscopy is also commonly performed by the paediatric surgeon. It is important that the lower lip is not pinched between the instrument and the teeth (or gums) and the upper teeth should be protected. These are excellent for teaching purposes. Fibreoptic examination of the nose. As large a size as possible is advantageous in order to obtain the widest view of the larynx. and the smaller ones can even be used for neonates. but it can be difficult owing to lack of cooperation in the awake patient. but this is withdrawn into the hypopharynx during laryngoscopy and the patient breathes spontaneously. paediatric endoscopy is indicated to provide a diagnosis in the presence of hoarseness and stridor. There is an increasing use of Hopkin rod telescopes with video and still documentation facilities. This gives a better view and suction is available. A wide abduction of the cords must be seen before normal cord movement is diagnosed.

p. p. p. The bronchoscope is passed down to the carina with examination of the walls to exclude a tracheo-oesophageal fistula. the tube is removed. If not. If there is a tracheostomy present. suprastomal granulations will nearly always be seen. Bronchoscopy A rigid telescope and bronchoscope of suitable size is introduced into the larynx with the help of McGill’s anaesthetic laryngoscope. In the normal patient the carina can be seen as soon as the instrument passes through the glottis. Stridor and stertor. An inability to see the carina when the lumen is apparently clear should raise suspicions of a vascular ring. and anaesthesia is then administered via the laryngoscope. 232. The main bronchus should be entered. The vocal cords are examined before passing the instrument gently through the glottis. 336. but it is often possible to pass the bronchoscope past the tube. This may not be possible if there is a high subglottic stenosis. Paediatric airway problems.238 OTOLARYNGOLOGY the laryngoscope at the same time and both oesophagoscopy and examination under anaesthetic of the nose may be indicated. . Tracheostomy. tracheomalacia or some other source of extrinsic pressure. During the removal of the endoscope the surgeon should continue to visualize the respiratory tract as damage is avoided and rarely a lesion is seen which had previously been missed. but more extensive investigation of the bronchial tree is necessary if a foreign body is suspected. 138. 311. Related topics of interest Laryngeal carcinoma. p.

which will help facilitate the development of speech and communication. intellect and motor abilities. This method is based on the presentation of a loud sound and observation of the baby’s response. Subjective hearing tests 1. family history. 5 years and over: pure tone audiometry. Listed below are the current screening methods of choice for the various age groups at which testing occurs. The choice of test will depend on the child’s age. Screening tests. Children failing both tests are referred for a more thorough audiological assessment. parental concern. Screening tests Hearing is important for normal speech development. Some experience is needed in interpreting the variety of possible .g. at 7 months. 4. The best results are achieved in multidisciplinary paediatric assessment centres where the environment and organization are geared for children. subjective hearing tests and objective tests are all available. post meningitis. Recent evidence has suggested that waiting until 7 months of age for a first screening test is too late. and it is important that moderate and severe hearing losses are diagnosed early. 2–4 years: distraction tests or conditioned response audiometry. Behavioural techniques (0–6 months). So called ‘Universal neonatal screening’ has therefore been proposed as a better solution. Most health authorities maintain an at-risk register of families in whom possible prenatal and perinatal causes exist. as will any child who persistently fails a screening test at any stage. 0. In an effort to achieve this aim. In addition. e. A thorough history from the parent or regular carer and a clinical examination are essential parts of the assessment. 2–4 years and again shortly after school entry.1% of live-born babies will have a severe hearing impairment. children in the UK have been subject to regular screening tests.PAEDIATRIC HEARING ASSESSMENT The assessment of hearing in children demands a variety of approaches which vary with the age of the child. This involves otoacoustic emission testing shortly after birth (the failure rate is reduced by waiting until after 48 hours of age). This will allow the provision of suitable support and aids. 3. 2. children may be referred for assessment from other sources because of concern about their hearing. Any failures are then subject to automated brainstem evoked audiometry. Nearly all subjective testing will require two testers. 1. Neonatal: Universal screening (OAEs with BERA if indicated). intensive care units (1–2% will have a severe hearing loss). 7 months: distraction test (see below).

g. behind and to one side of the child. A handheld audiometer may be used with older children. Evoked response audiometry. even if only at three frequencies in each ear. Sounds (warbles or pure tones) are produced from one of two loudspeakers placed at 30° either side of the child. cup/duck.240 OTOLARYNGOLOGY responses. and makes an objective verdict of pass or fail. sibilant s for higher frequency or a high-frequency rattle in younger children. Objective hearing tests 1. which include startle. startle responses and body movements are recorded by pressure transducers in the head rest and mattress. With this method it is important to avoid any visual cues. key/ tree. 2. This technique is relatively uncommon in the UK but more frequently used in USA and Australia. 4. In the McCormick toy test there are seven pairs with names that are acoustically very similar. A microprocessor analyses the responses to the sound stimuli. Respiratory changes are monitored by a transducer in a band around the baby’s chest. Conditioned reflex (performance testing) audiology (24–60 months). Head turning. or if the child is too young for conventional testing and there are doubts . The tester then distracts the child by making sounds of various intensity. A positive response is one in which there is a significant alteration in activity. Distraction techniques (6–18 months). A positive response is when the child turns to the sound. The stimulus is 5-second bursts of 85 dB sound pressure level (SPL) sound made into earphones. Pure tone audiogram (60 months+). This area of testing has been largely superseded by otoacoustic emissions. without giving any visual cues. With the child sitting comfortably on his or her mother’s lap. 5. 2. The stimulus may be the spoken word or a tone produced by a handheld audiometer. Auditory response cradle (0–6 months). a flashing light) to reinforce the turning response. crying or the cessation of activity. 3. If the child turns to the correct speaker at signal presentation a visual (reinforcing) stimulus is presented adjacent to the speaker (e. taking account of the baby’s overall level of arousal. Only those toys that are recognized by the child are used and the aim is to establish the speech level that gives an 80% correct response rate. Otoacoustic emissions (0–12 months). after hearing a specific auditory stimulus. Much of the recent work with otoacoustic emissions is related to their feasibility as a screening tool for sensory hearing loss. In this way a reasonably accurate free field audiogram may be obtained. The procedure is repeated on both sides. e. Test sounds include conversational voice for low frequency. This is indicated if there is any difficulty or uncertainty in the results of conventional distraction techniques. The toys are selected so that their names cover a range of speech patterns. This technique may also be used with older children to obtain a pure tone audiogram. These tests involve asking the child to point to or handle a variety of toys. 3. This device monitors four behavioural responses to the production of sound. This technique is discussed in detail elsewhere (pure tone audiometry). Distortion-product otoacoustic emissions have been shown to be particularly effective at 4 and 8 kHz. This technique involves training the child to perform a specific task such as putting a marble in a cup. or giving a toy to the mother. The child sits in an acoustic room at a table (usually with a parent) and is allowed to play with some toys. Most children of around 5 years can with a little encouragement be persuaded to perform an audiogram. The tester sits outside the test room and observes the procedure through a one-way mirror. 6. Visual reinforcement audiometry (9–36 months).g. In essence it is a free-field audiogram. blinking. an assistant attracts the attention of the child. The use of evoked otoacoustic emissions has been recommended as a mainstay of universal screening programmes. Speech discrimination tests (24–60 months).

. Culpepper B. p. Paediatric Audiology 0–5 Years.PAEDIATRIC HEARING ASSESSMENT 241 as to the child’s hearing ability. Universal newborn hearing screening programs. Related topics of interest Evoked response audiometry. Further reading McCormick B. p. p. 254. London: Whurr. Pure tone audiogram. 78. Its use is also suggested for neonatal screening in infants failing an OAE screen. Otoacoustic emissions. 216. 6:346–351. 1998. 1992. p. Impedance audiometry. 128. Current Opinion in Otolaryngology and Head and Neck Surgery.

Pathology Squamous papillomas usually occur at any age from birth to 5 years. Laryngeal mucus is thought to behave as a protective blanket in some sites. obtain tissue for confirmatory histology and to assess the extent of the disease and potential risk to the patient’s airway. . Respiratory obstruction and increasing stridor are late manifestations of the disease process. where there is increased airflow. Investigations Endoscopy is required to establish the diagnosis. chondromas. particularly HPV types 6 and 11. It is thought that in some patients the disease is transmitted at the time of delivery from a mother infected with genital warts. Clinical features Hoarseness of voice or an abnormal cry is the usual presenting symptom. which may become activated to form a recurrent lesion. Treatment can also then be initiated. Aetiology The aetiology of laryngeal papillomas is now known to be infection of the epithelial cells with human papillomavirus (HPV). fibromas. Adenomas. Electron microscopy and immunofluorescent techniques have shown that human papillomavirus DNA is incorporated into the host’s cellular DNA. They may grow anywhere in the respiratory tract from the lips to the lungs. for example the interarytenoid area. crusting and irritation. The lesions have a predilection for points of airway constriction. drying. This partly explains the difficulty in curing the disease. Apparently normal mucosa cells adjacent to the papillomas also contain viral DNA. Polymerase chain reaction is now the most sensitive technique available to show evidence of HPV infection. The growths may present as scattered single lesions or clusters or as a huge exuberant mass.PAPILLOMA OF THE LARYNX Squamous cell papilloma is by far the commonest benign tumour of the larynx. haemangiomas and other neurogenic and mesodermal benign tumours are all rare and will not be considered further. They can be sessile or pedunculated and are characteristically non-keratinizing with a connective tissue core. anterior commissure and vestibular folds are the commonest sites of involvement. but the vocal cords.

without damaging the larynx in the process. This increases the remission rate to approximately 50% in patients below 16 years of age. Kashima HK. McGlennen RC et al. 1. Pilot trial of ribavirin for the treatment of laryngeal papillomatosis. two operations 4 weeks apart are required to avoid web formation. 325: 613–617. Tracheostomy should be avoided if possible as the papillomas can become implanted into the trachea and bronchi. Mounts P et al Long term response of recurrent respiratory papillomatosis to treatment with lymphoblastoid interferon alpha-nl. 15: 504–513. 153:245–248. and to wait for resolution of the condition. Isotretinoin therapy for recurrent respiratory papillomatosis. Head and Neck. Terry RM et al. Isotretinoin (13-cis-retinoic acid) produces a significant response in about two-thirds of patients. Donovan DT. Medical treatment Alpha interferon has been shown to significantly reduce the growth rate of papillomas in one-third of patients. Head and Neck Surgeons. Single papilloma Single papillomas are usually seen in adults. arising from the free edge of a vocal cord. If disease is found to involve the anterior commissure. 1994. Effective Head and Neck Cancer Management. 1991.PAPILLOMA OF THE LARYNX 243 Treatment The aim of treatment is to remove the papillomas as they appear. Archives of Otolaryngology and Head and Neck Surgery. It has been claimed that the antiviral drug ribavirin is a useful adjuvant to surgery. The patients should be followed up for 5 years because of the risk of recurrence and malignant change. 120:405–409. Taylor-Cooley LD. more than 1–2 monthly) laser treatment. Second Consensus. treating first one cord then the other. Follow-up and aftercare Laser laryngoscopy is repeated as often as necessary to preserve the airway and the voice in those cases which do recur. Radiotherapy was used in the past. It is liable to recurrence and malignant degeneration. Demonstration of human papillomavirus types 6 and 11 in juvenile laryngeal papillometosis by in situ hybridisation. Surgery is the most satisfactory treatment of this condition. . but further trials are required to substantiate this.e. Further reading Eicher SA. but should be avoided as it predisposes to malignant change. It is most likely to occur if the disease presents between the ages of 6 and 10 years and if the disease is confined to the larynx. 1987. The papilloma should be removed at direct laryngoscopy. Because of treatment side-effects and uncertain response these treatments should be reserved for cases requiring frequent (i. Journal of Pathology. New England Journal of Medicine. Remission can take place at any age and does not seem to be related to treatment. 2000. 2. The treatment of choice is the removal of all the lesions using a laser. and repetition of this procedure at intervals. Squamous cell carcinoma and verrucous carcinoma are also more likely to occur in adults if the patient smokes. 1993. Wilson J (ed). British Association of Otolaryngologists. to maintain a safe patent airway and laryngeal function. Leuenthal BG. or if the trachea and bronchi become involved.

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Related topics of interest Lasers in ENT, p. 147; Paediatric airway problems, p. 232; Paediatric endoscopy, p. 237; Stridor and stertor, p. 311.

PERILYMPH FISTULA

Definition A perilymph leak into the middle ear arising from a defect of the oval and/or round window. It should not be confused with labyrinthine fistula, which is a fistula in the cortical labyrinthine bone secondary to CSOM. It may or may not have eroded through the endosteum to cause a perilymph leak. Aetiology 1. Congenital middle and inner ear deformities, in particular Mondini’s dysplasia or when there is a malformed stapes superstructure. 2. Head injury. 3. Barotrauma. 4. Iatrogenic in particular following stapedectomy. Clinical features A congenital perilymph fistula (PLF) should be suspected in children with an unexplained fluctuating or progressive sensorineural hearing loss with or without vertiginous symptoms. An external ear deformity may occur with the middle and inner ear malformation. A similar history following a head injury, barotrauma or middle ear surgery should be regarded as secondary to a PLF until proven otherwise. Shea’s series of iatrogenic post-stapedectomy PLFs presented with a mild mixed hearing loss and occasional dizzy spells but in over 36000 otological operations he has not seen a spontaneous PLF. Schuknecht has never seen temporal bone evidence of a spontaneous PLF including the review of the temporal bones of patients reported by Kohut as having a PLF. The current consensus view now holds that a spontaneous PLF does not occur in an otherwise normal ear without the above risk factors. Investigations A high definition CT scan of the petrous temporal bone is mandatory in suspected congenital PLF. Many subjects demonstrate a minor or major aplasia (see congenital hearing disorders chapter), in particular an enlarged vestibular aquaduct or Mondini’s dysplasia. Eighty-five per cent of congenital PLFs will have anomalies of the stapes superstructure, incus, promontory or round window demonstrable on CT. It has recently been shown that 2 transferrin is found in all human CSF and perilymph but in the serum of only 1

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in a 100 subjects. In those where a PLF is suspected from the history but not confirmed by a tympanotomy, washings of the middle ear for 2 transferrin can be made. Difficulty arises in deciding whether CSF or perilymph is the responsible agent in head injury patients with a positive 2 transferrin test. Hazel has noted that positioning a patient with a suspected PLF with the affected ear uppermost often improves hearing thresholds presumably because little perilymph escapes due to gravity. Management The diagnosis of PLF can only be made at tympanotomy. Sixty per cent arise from the oval window, 20% from the round window, 20% both windows, and 20% are bilateral. The oval or round window should be plugged with a fat graft, temporalis fascia or a vein graft. This is held in position in oval window PLF with a stapes prosthesis provided the incus superstructure is not malformed. Fibrin glue and more recently the KTP laser have been suggested to properly anchor an oval or round window graft in position. Temporalis muscle may be used to splint a round window graft reinforced by fibrin glue. Follow-up and aftercare Bed rest in the sitting-up position for 2–6 weeks is recommended as is avoiding straining or flying for three months. Diving is contraindicated. The patient is advised to cough or sneeze with the mouth open to reduce the chance of air entering the Eustachian tube and displacing the graft. One week of antibiotic cover is recommended. Further reading
Shea JJ. The myth of spontaneous perilymph fistula (Editorial). Otolaryngology Head and Neck Surgery, 1992; 107: 613–616. Schuknecht HF. Myths in neurotology. American Journal of Otolaryngology, 1992; 13:124–126. Kohut RI, Hinojosa R, Ryu JH. Perilymphatic fistulae: a single-blind clinical histopathologic study. Advances in Otorhinolaryngology, 1988; 42:148–152. Bassiouny M, Hirsch BE, Kelly RH, et al. 2 transferrin application in otology. American Journal of Otolaryngology, 1992; 13:552–555.

Related topics of interest Labyrinthitis, p. 134; Chronic suppurative otitis media, p. 38; Cholesteatoma, p. 35; Osteosclerosis, p. 223.

PHARYNGEAL POUCH

Diverticula of the pharynx are uncommon. The term pharyngeal pouch refers to a posterior pharyngeal pulsion (Zenker’s) diverticulum, and this has an incidence of approximately 1 case per 200 000 population per year. Other diverticula are very rare but include congenital lateral diverticulae, pharyngoceles and posterolateral pharyngeal diverticula. Aetiology and pathogenesis The cause of pulsion diverticulae is unknown. They arise posteriorly by herniation of the pharyngeal mucosa through a relatively unsupported part of the posterior pharyngeal wall known as Killian’s dehiscence. This weak area is at the lower part of the inferior constrictor muscle and is bound superiorly by the thyropharyngeal fibres and inferiorly by the cricopharyngeal fibres of this muscle. The pathogenesis is probably multifactorial, in part the result of a weakness at Killian’s dehiscence, incoordination of the pharyngeal phase of swallowing and cricopharyngeal spasm causing high intrapharyngeal pressure. A hiatus hernia and gastro-oesophageal reflux are sometimes present. Once a pouch is formed, food enters it and stretches it even more so that it enlarges. It may remain static for many years or slowly increase in size until it eventually passes into the posterior mediastinum. When the pouch reaches a moderate size it lies in line with the oesophagus and food may enter it preferentially. Pressure from the pouch may then be exerted on the oesophagus from behind to cause dysphagia. Clinical features Pharyngeal pouches are most frequently seen in the elderly. They cause a sensation of a lump in the throat, long-standing dysphagia, regurgitation of undigested food, halitosis, weight loss and recurrent chest infections due to aspiration. Hoarseness is unusual, but may occur as a result of irritation of the vocal cords from repeated aspiration or more rarely as a result of involvement of the recurrent laryngeal nerve by a carcinoma arising in the pouch. Rarely, a pouche may have an invasive squamous cell carcinoma in its wall. Swelling in the neck may be present and is nearly always on the left side. It may gurgle on palpation (Boyce’s sign) and empty on external pressure. 1. Radiology. A lateral plain film of the neck may reveal an air bubble in the pouch, but the definitive investigation is a barium swallow, which demonstrates the pouch. 2. Endoscopy. Oesophagoscopy should be carried out to exclude the presence of carcinoma. The instrument usually enters the pouch and an anterior bar may be seen separating it from the oesophagus. This investigation is often performed immediately prior to surgical excision of the pouch. In such instances a

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nasogastric tube is passed and the pouch is packed with proflavine gauze after any debris has been sucked clear. This will aid identification of the pouch during surgery. Management 1. No treatment Each case must be judged on its individual merits, with the patient being fully aware of the possible complications and potential benefits of operation. No treatment is indicated for a diverticulum which is causing few symptoms or in patients who are old, infirm and in poor general condition. 2. Endoscopic dilatation of the cricopharyngeal sphincter with bougies is only temporarily effective in relieving symptoms. It does not remove the diverticulum, which results in an eventual recurrence, and there is a risk of perforating the sac. 3. Endoscopic division of the bar between the pouch and the oesophagus. This can be performed with scissors or diathermy (Dohlman’s procedure). It is a quick procedure and a reasonable treatment for the frail and the elderly. The procedure does not remove the pouch, but it relieves the symptoms and restores swallowing by dividing the cricopharyngeus and widening the mouth of the diverticulum. The major risks are haemorrhage, mediastinitis, surgical emphysema and later stenosis. Amendments to the approach include the introduction of a specialized endoscope with a split beak. Endoscopic staple guns (which divide the wall and staple it synchronously) are now commonly used. This is the treatment of choice in nearly all pouches as results are good, morbidity low, and hospital stay short. 4. Pouch inversion. In this procedure a cricopharyngeal myotomy is performed and the pouch is mobilized, and then invaginated into the oesophagus and its neck oversewn with vicryl sutures. This operation avoids the risks of opening the sac, has a low complication rate and requires only a short hospital stay. This is the preferred treatment for small pouches. 5. Diverticulectomy. Excision of the diverticulum combined with a cricopharyngeal myotomy has remained a treatment of choice for many years. It now tends to be used for the very large pouches or when one of the other approaches has failed. The operation is performed in two stages, the first of which is the oesophagoscopy and the second the external approach to excise the pouch. Nasogastric feeding is continued for 5–7 days postoperatively, after which fluids are given. If there are no problems the tube is removed and a soft diet can be commenced the next day. Complications 1. Immediate. • Primary haemorrhage. • Surgical emphysema (mucosal tear or incomplete suture line). • Pneumothorax. 2. Intermediate. • • • • • Secondary haemorrhage (infection). Hoarseness (recurrent laryngeal nerve damage). Wound infection. Fistula (usually the result of infection). Mediastinitis (leak tracking downwards).

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3. Late. • Persistent hoarseness (recurrent laryngeal nerve divided). • Stricture (too much mucosa excised when dividing the neck of the sac). • Recurrence (endoscopic diathermy 7%, diverticulectomy 2–3%). Further reading
Bowdler DA. Pharyngeal pouches. In: Scott-Brown’s Otolaryngology, vol. 5, 6th edn. Hibbert (ed.) London: Butterworths, 1997: Chapter 10. Parker AJ, Hawthorne MR. Endoscopic diverticulotomy versus external diverticulotomy in the treatment of pharyngeal pouch. Journal of the Royal College of Surgeons of Edinburgh, 1988; 33:62–64.

Related topics of interest Globus pharyngeus, p. 113; Hypopharyngeal carcinoma, p. 124.

PHARYNGOCUTANEOUS FISTULA

Definition A fistula is an abnormal communication between two epithelial-lined surfaces. A pharyngocutaneous fistula is an abnormal tract joining the pharynx to the skin of the neck. Pathology Fistulae are unlikely after closed pharyngeal surgery but may occur following open surgery to the head and neck in which the pharyngeal mucosa has also been damaged. Consequently, laryngectomy is the most commonly associated procedure, but it may occur after pharyngeal pouch surgery, partial pharyngectomy or major oropharyngeal procedures (e.g. commando operation). Risk factors are: • Previous radiotherapy. • Infection (a persistent cough from a chest infection will put strain on the repair, and infection of the operated site will cause necrosis of the affected tissue with a leak through this defect). • Postoperative haematoma/chylous fistula/seroma. • Residual disease. • Poor nutritional status. • Poor surgical technique. Clinical features The patient most commonly develops a pyrexia 3 or 4 days postoperatively, associated with cellulitis of the neck wound. A swinging pyrexia and abscess formation may ensue. Typically on the seventh day the collection will rupture and a fistula will form. At this stage there will be a discharge of mucopus and the patient’s general condition will improve. In time, the discharge will become more mucoid than purulent and ultimately saliva alone is discharged. In many cases spontaneous resolution will occur, usually within 6 weeks. In persistent cases, especially in those having residual tumour or previous radiotherapy, there is the uncommon but ever present spectre of a carotid blow-out.

no surgical intervention is necessary. the diagnosis may be confirmed by a gastrograffin swallow. Two flaps are often needed because it is important to line the mucosal and cutaneous surfaces with skin. a local rotation skin flap should be considered in the first instance. In most cases the sinus will have resolved. The size of the external opening of the fistula should thereafter be measured weekly. Occasionally a fistula occurs several days after commencing oral feeding in patients who have had an apparently uncomplicated postoperative course. a choice of: a pectoralis major myocutaneous flap. It is suggested that nasogastric feeding be continued in this group for a further week and the gastrograffin swallow thereafter repeated. however. Those who have had surgery for benign disease are unlikely to develop a stenosis. Provided that the fistula continues to reduce in size. If the size does not reduce over any 2week period after the initial separation stage. and it is this group who are at a significantly higher risk of developing such a fistula. especially from a red fluctuant swelling in the neck. although granulation tissue should be biopsied to exclude recurrent disease in cancer patients. This may settle after several dilations. Management A pharyngocutaneous fistula is initially managed conservatively. With persistent and profuse discharge from a fistula. The repair method of choice is a microvascular jejunal loop because of its low morbidity and mortality compared with a gastric transposition. because local tissue is relatively ischaemic either as a result of previous radiotherapy or because of scar tissue formation during healing. After rupture. Nasogastric or gastrostomy feeding continues until the fistula has healed. These often fail. . The fistula may take many weeks to close spontaneously. and if personal and home circumstances are suitable the patient can be allowed home and reviewed regularly in outpatients. but followup for a year to exclude a late onset would seem sensible. if the tract is small. a deltopectoral flap or a radial forearm fasciocutaneous microvascular flap. but occasionally the stenosis recurs persistently and frequently so that excision of the affected segment with reconstruction is indicated. Follow-up and aftercare Patients who have had surgery for a fistula are followed up at the same interval as those who did not develop a fistula. The wound should be cleaned regularly and absorbent dressings used to avoid maceration of the surrounding skin until all necrotic tissue has separated and healing has started. although they are at a higher risk of developing a stenosis at the level of the fistula. a prudent plan would be to endoscope the patient under a general anaesthetic to exclude recurrent disease then to proceed with a repair. but if not the process is repeated until healing is complete. If the fistula opening is less than 1 cm diameter. electrolytes and serum proteins should be checked regularly and the haemoglobin kept above 10 g/dl. the urea. the repair method of choice is. If a local flap fails or the defect is too large to consider this. depending on the surgeon’s experience and microvascular training. this initial stage taking 2 or 3 weeks.PHARYNGOCUTANEOUS FISTULA 251 Investigation The diagnosis will be strongly suspected from the clinical features. A gastrograffin swallow performed on the 10th to 12th postoperative day will show an anterior sinus in about 15% of patients.

Management of Head and Neck Cancer. 203. 1993. McCombe AW. p. Reconstructive surgery. Radiotherapy. p. 267. Philadelphia: J. Cassisi NJ (eds). Related topics of interest Hypopharyngeal carcinoma.252 OTOLARYNGOLOGY Further reading Stringer. SP. p. In: Million RR. Laryngectomy.B. p. 124. 107:130–132. . Oropharyngeal carcinoma. Journal of Laryngology and Otology. 143. 1994:157–169. Flaps and grafts for reconstruction. 264. 2nd edn. Radiotherapy and complications of laryngectomy. Lippincott. p. Jones AS.

atrophy of the stria vascularis and microangiopathy can lead to metabolic upset and further cell death. Hearing loss in a young patient. Men and women are both affected. This can lead to secondary neural degeneration in the spiral ganglion. Clinical features Moderate hearing impairment (45 dB hearing level averaged over 0. there is a progressive degeneration in the auditory system with ageing. impairment. so that they find conversations difficult to follow. asymmetry on a pure tone audiogram. 1. rather than a sensory or neural. Circulatory changes such as arteriosclerosis. Presbyacusis is defined as the lessening of the acuteness of hearing that characterizes old age.PRESBYACUSIS As with all sensory systems in the human body. Cellular degeneration gives rise to a reduction in the numbers of inner and outer hair cells. Peripheral degeneration is reported to be responsible for at least two-thirds of the clinical features of presbyacusis. The end result in most instances will be a combined sensorineural. Patients typically complain of difficulty in hearing which is worse in the presence of background noise. Pathophysiology Both the sensory peripheral (cochlea) and central (neural) components of the auditory system are affected and the deterioration appears to become more rapid with increasing age. Many patients eventually become socially isolated and even depressed. Recruitment is a frequent problem and adds to the distortion. unilateral tinnitus or a conductive component to the audiogram will require investigation in its own right. depending on . although men tend to have a slightly worse loss for the same age group. Degeneration in the central pathways leads to a reduction in performance in terms of signal processing. In the absence of any other otological pathology the clinical examination is normal bar the hearing loss. which leads to hearing impairment in the affected individual. 2 and 4 kHz) occurs in 4% of the age group 51–60 but in 18% of those aged 71–80. little further investigation is required. This leads to an elevation of hearing thresholds and a loss of frequency selectivity. Although several different audiological patterns of hearing loss have been described. MRI scanning may be necessary to exclude an acoustic neuroma in any patient thought to be at risk. Investigations In the presence of an appropriate history and a symmetrical sensorineural hearing loss on pure tone audiometry. A variety of possible mechanisms exist.5. particularly at the basal end of the cochlea.

Hearing in ageing: issues old and young. Follow-up and aftercare Audiological support is initially required to familiarize and rehabilitate the user with the aid. The European Concerted Action Project. Current Opinion in Otolaryngology Head and Neck Surgery. Hearing in the aged. access is required for repairs and replacements.254 OTOLARYNGOLOGY the predominant histological changes. Some patients may be helped by rehabilitation in the form of speech reading or auditory training. Davis A. Any difficulties the patient might have can then be identified and dealt with. Rehabilitation. Suppl. only 18% of the elderly with hearing loss have and use hearing aids. There are several reasons for this. Management As there is no curative treatment for deafness associated with ageing. Simon HJ. the main aims in management are to assess the degree of disability. which may be dictated by further hearing deterioration with the passage of time. In the longer term. The sound is transmitted by induction from a special attachment and is picked up by the patient’s aid when it is switched to the T position. perhaps because the patient experiences some of the difficulties outlined above. 1999. 476. Many hearing aids dispensed are not used. Some patients have minimal handicap from their hearing difficulty despite a significant loss and therefore do not present themselves to medical services. Hearing aid uptake may be improved by the proposed introduction to the NHS and improved performance of digital hearing aids. Obtaining a hearing aid has become less of a problem for many patients since the introduction of direct referral schemes from general practice. . The role of rehabilitation and its benefits for the average hearing-impaired individual are not proven. G. It is likely that this aspect is the most important in hearing aid provision. Hearing aids. 1. Further reading Browning GG. Accessory aids. in general a sloping high-frequency loss is the commonest pattern found. 31:217–223. 1991. An induction coil fitted to the telephone or television may help some patients. This system is now available in many public places such as churches. concert halls and lecture theatres. Salomon. In some centres patients provided with a hearing aid are not seen again. including denial of hearing impairment. Follow-up and appropriate support for all patients issued with a hearing aid should be mandatory. Although about 75% of hearing aid users are over the age of 60. 1983. vanity. 3. 7:282–289. Clinical characterisation of the hearing of the adult British population. 2. In those with neural presbyacusis poor speech discrimination may limit the benefit of amplification as may the performance of the aid itself. Divenyi PL. to provide a hearing aid and rehabilitate the patient. The ENT surgeon or audiologist therefore has no idea if the patient has benefited from the treatment. Acta Otolaryngologica. Advances in Otorhinolaryngology. acoustic feedback and difficulty with manipulating the aid.

78. 192. Noise-induced hearing loss. p. . Pure tone audiogram.PRESBYACUSIS 255 Related topics of interest Evoked response audiometry. 254. Hearing aids. 117. p. p. p.

. It is measured in relative terms (dB ISO). Sound pressure level scale (dB SPL).3. In terms of pressure. The auditory system is less efficient at detecting sounds at the upper and lower ends of the frequency spectrum than in the middle regions. Hearing level scale (dB HL or dB ISO). and is measured in W/m2. It is a psychoacoustical test which aims to establish the subject’s pure tone hearing threshold. The clinical audiogram therefore gives an estimate of the subject’s hearing relative to normal.3-fold increase in sound pressure. but the perception of only doubling the loudness. not to equal increments. A decibel scale of human hearing was designed so that 0 dB hearing level (HL) would be the expected threshold of detection of a pure tone irrespective of its frequency. intensity is exponentially related to loudness perception and therefore a logarithmic scale to measure loudness is necessary. This standard represents the thresholds at each test frequency for a group of presumed otologically normal young adults. Decibel scales 1. that is the minimum sound level at which a specific response can be obtained. In the dB HL scale normal hearing individuals would be expected to have a flat audiogram. the threshold of hearing corresponds to a sound pressure level (dB SPL) of approximately 20 x 10–6 pascals and the threshold of pain to a level of 200 pascals.PURE TONE AUDIOGRAM The pure tone audiogram is probably the cornerstone of clinical auditory assessment. The decibel is 10 times this ratio. a 3. Therefore: Sound intensity (Ix) in dB=10 log10 Ix/Io where Io=10–12w/m2 Since sound intensity is proportional to the square of the sound pressure then: Sound intensity in dB=10 log10 sound pressure2 or = 20 log10 sound pressure level Log10 2 is about 0. but to equal multiples of sound intensity. 2. The amount of energy at 0 dB HL at each frequency is not the same. where the reference zero is an internationally agreed standard. so doubling sound intensity corresponds to a 3 dB increase. It was considered that the use of a dB SPL scale in pure tone audiometry would make abnormalities difficult to identify. The bel is the log to the base 10 of the ratio of the sound intensity being measured to a reference intensity which is constant. The detection of sounds in decibels of sound pressure level (dB SPL) produces a pure tone audiogram which in normal circumstances would not be flat. In other words. Introduction The ear responds equally. the mean level being 0 dB HL. Each 10 dB increase represents a 10-fold increase in the intensity of sound (log1010=1).

If the middle-ear defect is corrected. 2000 and sometimes 4000 Hz for bone conduction. 500. Masking Masking is the phenomenon by which one sound impairs the perception of another. it is not an absolute representation of inner ear threshold. Pure tones are produced by a calibrated audiometer and are first presented to the subject’s better ear. Background Pure tones of several frequencies are tested. with a standard error of 3–5 dB. Bone conduction is taken to give an indication of cochlea function. 1000. The results of bone conduction become less reliable at and above 4000 Hz. 2000. Method The subject is seated in a soundproof room and the procedure is explained by the examiner. Smaller steps could be used (e. 4000 and 8000 Hz for air conduction (although 3000 and 6000 Hz will be required for noise-induced hearing loss claims) and 500. This causes an artificial depression of the bone conduction thresholds whenever a conductive defect is present. For this reason 5 dB steps are used for clinical audiometry.g. 1000. Earphones are used for air conduction and the subject is asked to signal by pressing a small hand-held button as soon as the tone is heard. Thresholds are ascertained using a psychophysical method of limits. The ear is not equally sensitive to sounds of different frequencies. 2000. To take account of this an’ A. This continues in the following order: 1000. but because a variety of routes for the transmission of sound to the cochlea exist for bone conduction. . and at 250 Hz are often not representative as they may be felt rather than heard. Tones are first presented at an intensity above the patient’s suspected threshold. 8000.weighting’ is used. When the skull is set in vibration by a bone conduction vibrator. In the context of pure tone audiometry. The intensity is reduced in 10 dB steps until no sound is heard. The second ear is then tested in identical fashion. The timing and duration of signal presentation should be varied and no visual clues should be offered. 4000. 2 dB) but the procedure would be markedly prolonged without significantly improving accuracy. With any psychoacoustic test there is a variation in the results obtained in any test-retest situation. This has become known as the ‘Carhart effect’ after he described it in patients who had successful fenestration surgery for otosclerosis. This overcomes any cross-hearing (the interaural attenuation for air conduction is of the order of 40–60 dB when wearing headphones) and allows an accurate assessment of the true threshold of the test ear for either air or bone conduction. the sounds reach the inner ear by the direct osseous route or via transmission across the middle ear. It is particularly sensitive to sounds in the ‘speech frequencies’ (500–4000 Hertz) and progressively less so to sounds of lower and higher frequencies. which reduces the contribution of very low and very high frequencies to the overall noise level measurement. 500 and 250 Hz. masking is used to raise the threshold in the non-test ear using air-conducted sound. This dB A scale is used in industrial and other noise exposure settings. The signal is then increased in 5 dB steps until half of the tone pips are consistently heard. Finally 1000 Hz is tested again to check on subject accuracy and should be within 10 dB of the first result. usually 250. In addition it appears that the ear is less easily damaged by the sound frequencies to which it is less sensitive. then the bone conduction thresholds will appear to improve because of the addition of the middleear component.PURE TONE AUDIOGRAM 257 3. The A-weighted scale (dB A).

narrow band noise with a central frequency identical to the test tone is used. the method has fallen into disuse for most other problems because it is too unreliable. This variant uses a special audiometer which automatically sweeps from low to high frequencies while presenting continuous or pulsed tones. Recommended procedures for puretone audiometry using a manually operated instrument. (b) Air conduction studies whenever the unmasked bone conduction is 40 dB or more better than the worse air conduction. Although still used for screening industrial hearing loss. 15:213–216. The subject alters the intensity of the tone by pressing a button if the tone is heard which lowers the intensity of the signal. In: Clinical Otology and Audiology. continuous/pulsed tones) additional diagnostic information about adaptation. but if the result is unusual it will require manual confirmation. it is ideal for workforce screening. 192. The masking level in the non-test ear is determined by shadow masking and recording the thresholds on a masking chart. . 1981.g. recruitment and nonorganic hearing loss can be provided. By varying the test technique (e. Leijon A. Non-organic hearing loss. Variations 1. 2. forward/backward sweeps. Bekesy audiometry. Further reading British Society of Audiology/British Association of Otolaryngologists. In essence this is identical to the above but a microprocessor presents the tones and analyses the responses against predetermined values. London: Butterworths. British Journal of Audiology. 194. p. It is useful as a screening test and in very busy clinics. There are three scenarios when masking is essential: (a) Masking must be applied to the better ear when testing air conduction in the deafer ear if the difference in unmasked thresholds is found to be 40 dB or more (to prevent interaural attenuation). 1992. Related topics of interest Noise-induced hearing loss. Browning GG. The masking noise is delivered by an ear insert for bone conduction and headphones for air conduction. Audiometric tests. Quantization error in clinical pure-tone audiometry. 21:103–108. 1986:38–47.258 OTOLARYNGOLOGY As masking is most effective when the frequency of the masking noise overlaps the test tone. Thus a zig-zag printout is obtained from which thresholds at each frequency can be estimated. Scandinavian Audiology. Computerized pure tone audiometry. When the signal cannot be perceived the button is released which increases the intensity again. p. As the test can be self-administered and provides an automatic printout. (c) Bone conduction testing whenever the unmasked bone conduction is 10 dB or more better than the worse air conduction.

Motility disorders are best assessed using dynamic video swallow fluoroscopy. Lateral soft tissue views of the neck are of limited value in isolation. but many foreign bodies are likely to be non opaque. Water soluble contrast swallows (using non ionic relatively inert contrast media) are indicated when the history suggests that aspiration into the lungs is a real risk (if barium is used in these circumstances it may lead to resistant chest infection or permanent lung damage). Unenhanced CT scans are usually performed for the assessment of benign sinus disease prior to functional endoscopic sinus surgery. The radiation dose of a 4 projection sinus series is equivalent to 25 chest X-ray doses or 10 weeks of background radiation. Digital screening is preferred to reduce radiation dose. Contrast swallow A contrast swallow is indicated in the investigation of dysphagia or symptoms suggestive of motility disorders. The Royal College of Radiologists’ guidelines recommend that ‘plain films of the sinuses are not routinely indicated’. and of the temporal bone for assessment of bony . Contrast swallows are more accurate in this situation. Image acquisition is preferably at the rate of 2 frames per second during a bolus swallow. when perforation of the oesophagus is suspected or a surgical anastamosis is being evaluated (barium used in these circumstances will remain in the soft tissues if a leak is present. obscuring the area for further follow up studies and being a viscous thick suspension it is less likely to demonstrate small oesophageal leaks than water soluble contrast). plain films are rarely used for diagnostic purposes in ENT.Lewis-Jones Diagnostic imaging techniques Plain films Following the increased use of complex diagnostic techniques such as CT and MR. They may demonstrate opaque foreign bodies. Barium swallows are of superior sensitivity in demonstrating pharyngeal pouches. Computerized tomography CT provides vastly improved delineation of bony structures and of soft tissue structures of the head and neck compared with plain films.RADIOLOGY IN ENT H. pharyngeal webs (the web is a line indenting the anterior aspect of the barium column at the level of C5/6) and cricopharyngeus hypertrophy (indents the posterior column of barium at the C6/7 level).

Gadolinium is a paramagnetic contrast agent used in MRI It behaves in exactly the same way as iodine based contrast media described in the CT section. in abundance in the body. and also of demonstrating abnormal areas of enhancement. This is particularly useful in oncology and in complex anatomical evaluation of the temporal bone. The fundamental imaging unit in MR is the proton or hydrogen nucleus. One of these components. and it also relates the MR characterization to CT appearance. which has the benefit of opacifying blood vessels making lymph node enlargement easier to detect. but important. but provide better contrast for the detection of abnormal tissues such as tumour or inflamed tissue. These characteristics are represented in T1 or T2 weighted imaging sequences. and this causes abnormal tissues to enhance (appear white). which when placed in a strong magnetic field act like small metallic dipoles and align predominantly in the direction of the magnetic field. represent the biochemical composition of tissues in the body and it is this concept of tissue characterization through MRI that makes soft tissue delineation so superior. is related to the time taken for excited spinning protons to return to their normal position in the magnetic field. the T1 spin lattice or longitudinal relaxation time. Table 1 below shows patterns of tissue characterization. In abnormal tissues it leaks into the intra cellular compartment. The T2 weighted images tend to provide lower resolution images in terms of anatomy. Intravenous contrast usually flows from the vascular compartment into the extra cellular compartment. the T2 spin spin or transverse relaxation time. T1 weighted images are used to demonstrate enhancement (an increase in signal) with gadolinium. Enhancement of an area directly indicates its vascularity and the degree of enhancement shown in MRI is in the range of 50–100 times greater than that shown in CT. . A final. Energy in the form of a radio wave is transmitted into the body at a precise frequency causing the protons to resonate. depends on excited spinning protons moving out of phase with each other as they relax. The images generated. This creates images with a T2 weighting. where observation of signal on T1 and T2 weighted images allows identification of tissue type.260 OTOLARYNGOLOGY anatomy. The resonant radiowave is then turned off and protons gradually relax back into the direction of the magnetic field giving off a radiowave which is detected as the MR signal. whereupon they realign in a direction against the magnetic field. This leaves pathology and fluid including oedema as white in the image and more conspicuous than in ordinary T2 weighted images where high signal fat may well obscure the boundaries of a tumour. In tumour work it is routine to administer iodine based intravenous contrast. but with fat signal suppression. Modern multi-slice CT scanners can now acquire data volumetrically allowing multi-planer recontruction of CT images. therefore. Magnetic resonance imaging MRI provides markedly superior delineation of soft tissues in any imaging plane. CT is disadvantaged in the densest part of the skull base where artefacts are commonly caused in the adjacent soft tissue due to X-ray absorption in dense bone. the STIR sequence. but not into cells. T1 weighted images provide high resolution of anatomy and excellent soft tissue detail. The only exception to this rule is in the brain where the blood-brain barrier prevents contrast flowing into the extra-cellular compartment also. more conspicuous. Pathological enhancement in the brain is. This sequence is of great value in the delineation of head and neck cancers. The MR signal given off by protons can be detected and resolved into two different components. set of MR images is worthy of mention. The second. therefore. The T2 weighted images are good at detecting abnormal biochemistry related to abnormal tissues.

The high resolution T2 weighted technique must identify the normal facial and acoustic nerves separately within the internal acoustic meatus to successfully exclude small intracanalicular neuromas. in particular. This will provide evidence of abnormal appearance at this . Correlation of MR and CT appearances of tissues MR cannot be used in patients with cardiac pacemakers. Ultrasound Ultrasound is a very useful technique for the assessment of masses in the neck. certain cardiac prosthetic valves. It does not involve any radiation exposure and can be linked with ultrasound guided fine needle aspiration.RADIOLOGY IN ENT 261 Table 1. 2. performed as an outpatient procedure at the time of diagnostic scanning. This provides superb bony detail of both the inner and middle ear structures. It is also used for specific cases following MRI (see below). It is indicated as the first line choice of radiological investigation when chronic middle-ear disease is being investigated. in the first trimester of pregnancy. involve a high radiation dose (100 chest X-ray-equivalents or 1 year background radiation). iron containing brain clips. it is very operator dependent requiring an ultrasonologist with specific technical skills who performs head and neck ultrasound regularly. thyroid goitres and for suspected salivary gland pathology. ENT pathology Temporal bone disease The choice of investigation rests between CT and MRI. 1. Developmental anomalies including vestibular aqueduct dilatation can usually be identified on a high resolution T2 weighted MRI.5–10 mHz) hand held probe is placed directly on the neck and the fine needle can be visualized directly entering individual lesions as small as 1 cm in diameter. however. bone algorithm. MRI. when the diagnosis of cholesteatoma is suspected. High resolution CT (1 mm slices). however. for trauma induced deafness and suspected otosclerosis. or in patients with cochlear implants. As a technique. High resolution T2 weighted MRI of the temporal bone is now the accepted screening tool for patients with suspected acoustic neuromas although gadolinium enhanced MRI remains the gold standard for detection of small acoustic neuromas. A high frequency (7. It does.

Skull base and nasopharynx. 3. All anatomical variants should be identified. Multi-planar MRI with gadolinium enhancement is the first line investigation supplemented with high resolution CT if focal bone destruction is suspected. predominantly as it minimizes movement/swallowing/breathing artefact. Oral cavity and oropharyngeal tumours.262 OTOLARYNGOLOGY site. onodi cells next to the optic nerve. This does not require arterial or venous catheterization or even intravenous contrast. The plain film OPG allows accurate detection of dental caries which can cause increased activity on the isotope bone scan (and otherwise a false positive result). low lying or asymmetrical cribriform plate. The scans would identify the pattern of sinus disease. e. allergic sinus disease associated with nodular and irregular mucosal thickening+or—polyposis). but a tumour should be excluded. 2. MRI is accurate at showing vascular occlusion or encasement by tumour. Spiral CT is regarded as superior. Head and neck cancer 1.g. In equivocal cases MR angiography or venography is indicated. CT also appears superior to MRI in the detection of early thyroid cartilage invasion (this is seen initially as some . This involves: • Coronal images 2 mm cuts every 8 mm from anterior frontal sinus to posterior border of sphenoid sinus. Moving blood can be specifically identified in an ultra fine slice and placed in a 3D matrix representing the vascular tree. Absence of caries associated with increased activity indicates bone invasion. High resolution T2 weighted MRI is also a useful screening test for evaluating congenital deafness. CT and MRI are comparable at staging tumours at this site. This technique is also of value in diagnosing cavernous or lateral sinus thrombosis. Bone destruction of the mandible is best evaluated using a combination of isotope bone scan with plain film. whether the cause is related to the osteo-meatal complex and its nature (inflammatory sinus disease associated with parallel walled mucosal thickening. Sinus disease CT is indicated following failure of medical treatment and on consideration of functional endoscopic sinus surgery. • Two axial cuts are also performed. secondary to orbital or mastoid infection. dehiscent roof of carotid canal in the sphenoid sinus. one through the frontal sinus to show the posterior sinus wall and the second through the apex of the orbital foramen to show the relationship of sinuses to the optic nerve. High radiation doses is a particular problem with CT of the sinuses and for this reason a low dose protocol is recommended. Bone destruction can be seen with polyposis and fungal disease. and supplemented by high resolution CT of the affected area if surgical treatment is contemplated. It may be necessary to recall the patient for images in the sagittal plane to allow accurate measurement of the vestibular aqueduct in equivocal cases. Differentiating oedema from tumour can be difficult. Hypopharynx and larynx. Destructive lesions of the temporal bone apex or elsewhere at the skull base should be imaged in all three planes. This is often clinically occult disease. particularly those which place vital structures under increased risk of damage during endoscopy. If a tumour is suspected. presenting with cranial nerve palsy or neuralgia. a contrast enhanced spiral CT or contrast enhanced MRI is indicated. The radiation dose is equivalent to 80 chest X-rays or 10 months of background radiation. Gadolinium enhanced MRI provides the superior soft tissue delineation required for defining the extent and spread of these tumours.

Ultrasound guided fine needle aspiration is the most accurate method of a radiological assessment of the NO neck. Recent studies have shown a high incidence of disease in the thorax. which is not detected by a plain radiograph. • All other nodes minimum axial diameter greater than 10 mm. then imaging or FNA of the nodes is of little value. as well as direct spread of tumour. Salivary gland pathology Control films with contrast sialography is still indicated for intermittent swelling of the major salivary glands. This will provide information regarding gland function and obstruction. retrolaryngeal lymph nodes. MRI is probably superior in this regard as it can reveal oedema in adjacent anatomy.RADIOLOGY IN ENT 263 sclerotic change within the cartilage before lysis occurs). again masked by post surgical or post radiotherapy fibrosis. 7. CT of the thorax is probably not indicated for T1 N0 tumours. not all involved lymph nodes in an NO neck will be detected and if neck dissection is routinely planned. and are biopsied using a fine needle. Failed procedures usually in the submandibular area can be referred for isotope sialography. and makes scan interpretation difficult. CT and MRI can demonstrate lymph nodes in the neck. Cervical lymph node assessment. 6. which by definition are at an early stage. but enlarged. . • Central necrosis: This is visible as cystic change within the lymph node and can be seen on all three modalities. Postoperative assessment. It is superior in the demonstration of small. 4. Radiotherapy creates a great deal of oedema which can last up to 12 months following treatment. The incidence of occult disease has been reported as high as 15%. It is suggested that CT scan of the thorax should be routinely performed in patients with head and neck cancer who have a normal chest X-ray. This gives an 85% sensitivity and 100% specificity for detection of tumour. The technique involves identification of the 3 largest lymph nodes in the ipsilateral neck. a baseline post-operative scan at 6 to 8 weeks is helpful. Recurrence may take the appearance of a focal occult mass lesion at the site of reconstruction or of clinically occult lymphadenopathy. either metastatic or a synchronous primary bronchial neoplasm. • Extracapsular spread: This is shown by attachment or invasion of adjacent structures. Distant metastases. although no other specific information will be obtained. Ultrasound. These criteria will provide approximately 60% sensitivity and 95% specificity for lymph node involvement by tumour. Stones and strictures can be treated percutan-eously under imaging guidance using micro angioplasty ballons and micro cages mounted on guide wires. If complex reconstructive procedures have been performed and there is a high likelihood of recurrence (close margins. There is 100% specificity for tumour involvement by squamous cell carcinoma. 5. Imaging has low specificity levels due to variable ossification of cartilage in normal life. more than one involved lymph node at pathology unfavourable histology). Even so. MRI has proven superior in detection of recurrence. • Grouping of more than three lymph nodes of 5–8 mm in one lymph node level. All three imaging modalities use essentially the same criteria for nodal involvement by tumour: • Jugulo-digastric node with minimum axial diameter greater than 15 mm. The NO neck. This is also the case in the post-operative larynx.

Mack M. 1999. The PA chest radiograph is the first investigation. Philadelphia: Saunders. p. Oral cavity carcinoma. Second Consensus. 180. Laryngeal carcinoma. Steger W. MR can provide superior information re: (a) Characterization of cysts or lipomas. Balzer J. Laryngeal nerve palsy Urgent endoscopy should be co-ordinated with radiological assessment. Differential Diagnosis in Head and Neck Imaging. Vogl TL. allowing prioritization for potentially malignant masses. Imaging of the Paranasal Sinuses and Oro-maxillo-facial Region. if necessary. by CT. 1995. New York: Theime Publishers. 197. Matee BL. British Association of Otolaryngologists. Further reading Valvassori GE. New York: Theime Publishers. 108. Imaging should always be combined with clinical assessment and fine needle aspiration of the mass. p. Related topics of interest Acoustic neuroma. 203. 2000. 1. p. (c) Extension of the mass into the deep lobe of the parotid gland. p. 124. Nasopharyngeal carcinoma. a spiral CT from skull base to the lower border of the lung hila is required. 138.264 OTOLARYNGOLOGY Salivary gland masses can be assessed. . Hypopharyngeal carcinoma. p. Oropharyngeal carcinoma. Imaging of the Head and Neck. p. Radiological Clinics of North America. Wilson J (ed). If endoscopy and the chest radiograph fail to identify the cause of laryngeal nerve palsy. p. Head and Neck Surgeons. Effective Head and Neck Cancer Management. MR or ultrasound. Imaging can usually successfully identify benign salivary gland lesions. (b) The pattern of homogenous enhancement or non-homogenous enhancement. Carter BL. 1993. FESS.

releasing energy. For treatment of head and neck cancer. 4. 2. They are used to boost the dose to a neck lump lying in close approximation to the spinal cord. with a rapid fall-off in dose beyond this.RADIOTHERAPY A. which may be particulate (usually electrons) or uncharged electromagnetic radiation called gamma rays. Biologic principles Factors that affect the response of cells to a given dose of radiation include: • Radiosensitivity is an inherent characteristic of the cell (e. seminoma and leukaemia cells are exquisitely sensitive to radiation whereas glioma and melanoma cells are relatively radio-resistant). converting their kinetic energy into heat and photons. They give a uniform dose up to a certain depth which varies depending on the energy of the beam. • Oxygen is a potent sensitizer. having the same wavelength and energy as X-rays. A photon is a quantum or bundle of electro-magnetic radiation. The technique is more skin sparing than orthovoltage radiotherapy and is the treatment of choice for irradiating the nose and pinna.. there is a relatively slow fall-off in dose with depth.g. Megavoltage linear acceleration of the electrons produces X-rays in the energy range of 4–20 MeV. Its role in head and neck cancer has yet to be defined but some authorities find it useful in the treatment of sinonasal and advanced salivary tumours. Energy The amount of energy of a photon beam is described by the roentgen (R). which are enhanced in melanoma cells. Oxygen enhancement ratio (OER) is the ratio between doses in hypoxic and euoxic cells to produce the same biologic effect. 5. there is significant scatter and the dose is more difficult to map precisely. 3. 1. while the gray (Gy) is the unit of absorbed dose by the tissues. Gamma rays Radioactive atoms disintegrate to form a more stable atom. Orthovoltage machines produce X-rays of about 300 kV. usually tungsten. They are produced when high-speed electrons expelled by thermionic emission from an electrically heated tungsten filament are arrested by a target anode of high atomic number. Electrons High-speed electrons can be used as an alternative to electromagnetic radiation. Neutrons These are produced by bombarding stable nuclei with electrons in a cyclotron. due to its ability to form free radicals.Shenoy Radiotherapy is treatment with ionizing radiation. This may consist of high-energy electro-magnetic radiation (X-rays and gamma rays) or particulate radiation (electrons (beta particles) or neutrons). energy of 4–6 MeV is used. X-rays X-rays have a smaller wavelength than UV light and have high energy: kilovolts (kV) to megavolts (MeV). OER for low . the maximum dose delivered is to the skin. However. This is to a certain extent dependent upon cellular repair mechanisms.

Malignant cells have a greater proportion of actively dividing cells (a larger growth fraction) and so a greater percentage of cells will die. Maximizing the therapeutic ratio is the overriding principle of radiation therapy. Many manoeuvres are utilized to maximize the ratio including fractionation of dose. There are however more complex differences between various normal tissues and it is important to realise that prolonging treatment time has little effect on late effects. Clinical principles Radiotherapy should be defined in terms of type. have a shorter cell cycle. allowing repair of damaged DNA before the next cell division. interval between fractions and volume treated. interstitial brachytherapy. for example iridium wires placed in flexible plastic tubes. multiple fields. five fractions per week over 5 to 7 weeks. and is the ratio between normal tissue complication dose to the tumour control dose. There are various methods of application in the head and neck including external beam therapy (teletherapy) using linear accelerators or cobalt isotope machines. the total dose delivered is about 10 to 15% higher than conventional . Normal cells are able to synthesize factors such as p53 protein.266 OTOLARYNGOLOGY energy X-rays is between 2. prolonging the S-phase (synthesis of DNA). method of application. are less likely to repair damaged DNA and more likely to undergo apoptosis before entering mitosis.e. Acceleration uses the same or slightly lower dose than conventional therapy with the same number of fractions delivered in a markedly reduced overall time. Altered fractionations use more than one fraction per day and are essentially divided into two schedules of accelerated fractionation and hyperfractionation. The adoption of fractionation into radiation has led to the concept of four ‘Rs’ of radiobiology. so that a small increase in dose may greatly increase tissue injury. Many tumours are thought to have hypoxic cores leading to radio-resistance. fraction size is the dominant factor in determining late effects in normal tissue. but a large sparing on early effects. Repair. Each tissue has its own tolerance level beyond which radiation toxicity will occur. iodine-131 for thyroid cancer). Repopulation. Hyperfractionation uses less than conventional dose fraction in the same overall time. S phase cells are relatively more resistant than M phase cells. both fraction size and treatment time determine response of acutely responding tissues.8–2 Gy per fraction. but because multiple fractions are used. Conventional fractionation is defined as treating once daily at a dose of 1. Omission of one or two fractions of radiotherapy. In contrast. As a result. perhaps because of acute side-effects.5 and 3. Redistribution and Re-oxygenation. can significantly reduce the chances of cure. use of lead alloy blocks (to reduce normal tissue included within the radiation fields) and use of wedges to alter the dose distribution. The principle is to provide a sufficient dose to the tumour to effect a cure or adequate palliation but provide a minimal dose to the surrounding normal tissue in order to minimize complications. while overall treatment time has little effect. Resting malignant cells have much less capability to arrest in S-phase. meaning the dose to hypoxic cells is three times greater than in oxygenated cells. DNA is most susceptible to lethal injury when the cell is dividing and is not able to repair DNA damage. • Linear energy transfer (LET) is the amount of energy deposited as the X-ray travels through matter. number of fractions. Dose fractionation spares normal tissues because of cellular repair in between fractions and due to repopulation if the treatment time is sufficiently long. The intent is to reduce repopulation in tumours. and systemic radioactive isotopes (i. A higher proportion of malignant cells will therefore die from radiotherapy. High LET radiation (neutrons) have a more biologic effect than low LET radiation (X-rays). The late effects are not reduced. Resting cells may also sustain DNA damage. as the fraction size is similar to conventional treatment. • The position a cell occupies in the cell cycle determines sensitivity to radiation. fraction size.

Two or more beams from different angles may be needed to obtain an adequate radiation dose to the tumour volume while maintaining surrounding tissue tolerance. Various trials have been performed which have demonstrated the clinical effectiveness of the above strategies and radiotherapy treatments using multiple fractions are being increasingly used in clinical practice. A computer maps out a plan of the dose applied to the tumour and surrounding structures by calculating the summation of the contributions of the applied beams modified by wedges. pharynx). p. desquamation.RADIOTHERAPY 267 treatment. p. the number of fractions and the total treatment time. localized cortical radionecrosis) and bone (osteoradionecrosis). Int. 197. eye. mucous membranes (mucositis. lassitude and anorexia. 48:7–16. Use of wedges that attenuate a beam’s dose differentially across its width helps this. J. Oral cavity carcinoma. volume treated. p. . blocks and compensators. Local side effects depend on the type of radiotherapy. 180. Oncol. Verification radiographs are taken during the first fraction dose and compared with the simulation films to ensure that the field is correctly positioned. p. Trotti A et al.. and atrophy of sweat glands and other skin appendages). Sinonasal tumours. p. 124. Nausea and vomiting are less common. A Radiation Therapy Oncology Group(RTOG) phase III randomised study to compare hyperfractionation and two variants of accelerated fractionation to standard fractionation for head and neck squamous cell carcinomas: first report of RTOG 9003. candidiasis and reduced saliva production due to minor salivary gland atrophy). Laryngeal carcinoma. The patient is immobilized in an individually made plastic head and neck shell. Related topics of interest Hypopharyngeal carcinoma. cartilage (perichondritis). Further reading Fu KK. 2000. 138. Pajak TF. These blocks are marked on the shell. Typically. Radiat. radiotherapy can damage skin (erythema. brain and spinal cord (transverse myelitis. Biol Phys. 280. the total dose. Nasopharyngeal tumours. Accurate targeting is essential due the close proximity of vital but radiation-sensitive structures (cervical spinal cord. Side effects General side effects include tiredness. A variable margin around the tumour is included to allow for microscopic involvement. On a simulator (X-ray machine with image intensifier) the field is chosen and lead alloy blocks used to protect vulnerable structures. Treatment planning Examination and CT or MR scanning defines the treatment volume.

McRae Reconstructive surgery is the surgical technique to replace tissue loss caused by trauma. Level 2 Skin grafts. The depth of plane varies according to site. The graft has no blood supply and so needs a vascular bed. refined anaesthesia and microsurgery have allowed more major head and neck resection procedures to be developed. A skin graft is less likely to take at sites of poor vascularity.D. Level 1 Direct closure. The skin is able to be stretched but its tolerance varies according to site and age. Manchot in 1889 studied the blood supply of the skin and introduced the concept of vascular territories. Excision of a lesion should be planned so skin incisions are in the line of least tension as mapped out by Langer’s lines.Niranjan and R. A skin graft is a segment of epidermis and dermis that has been completely separated from the donor site and thus has no blood supply. It will not take on bone without periosteum. Although skin cover could be achieved by staged transposition of tubed pedicled fasciocutaneous flaps from distant sites. The contact between the graft and recipient site is maintained by a pressure dressing or by the exposed method.R. The pressure dressing could a pressure bandage or a tie over dressing with foam or cotton wool. heavily irradiated tissue or on infected tissue. haematoma or a collection of pus between the graft and recipient site. for example on the face the level of undermining is very superficial but on the scalp it is deep to the galeoaponeurotica. The development of one-stage pedicled myocutaneous flaps and microvascular free tissue transfer over the last 25 years has largely removed these criticisms with the consequential enormous improvement in the quality of life for head and neck cancer patients. Skin suturing should be without undue tension. while in 1936 Salmon confirmed the distribution of the perforating branches from marginal arteries. In exposed wounds one needs to observe for a seroma. retention of function and quality of life were usually poor. We have classified reconstruction into four levels. It may be desirable to close small defects directly. for example over fat. Following the excision. On the trunk and limbs it lies between the superficial and deep fascia. In addition some procedures took over a year to complete.RECONSTRUCTIVE SURGERY N. They may be classified into split skin grafts (also called partial thickness skin grafts) or full thickness skin grafts (also called Wolfe grafts). The advent of antibiotics. cartilage without perichondrium or tendon without paratenon. it can be . cosmesis. tumours or congenital deformity. If a haematoma or seroma develops. undermining should be between tissue planes. These lines are usually at right angles to the underlying muscle fibres.

Examples include deltopectoral and nasolabial flaps. These are fasciocutaneous flaps with a named blood supply running superficial to the deep fascia supplying the overlying skin. A random flap is one where there is an indirect or an unknown direct blood supply to the skin. It should be noted that the dermatome scale acts as a guide only: other factors such as angle of the dermatome to the skin and skin tension will alter the graft thickness.5 mm is recommended for covering within the oral cavity.3– 0. (b) A full-thickness graft with all adipose tissue excised is ideal when performing a septodermaplasty. Immediate grafting with quilt suturing and cross-hatching of the graft is recommended so that blood and serum can escape and do not lift the graft from its bed. rhomboid. Examples of random skin flaps are Z-plasty. They can be classified into random. The pectoralis major myocutaneous flap has replaced many of the indications for the deltopectoral flap. but the troughs of the rete pegs and epithelium lining the hair follicles are left in situ to allow re-epithelialization of the donor site should be harvested using an electric dermatome set at 3 or 4 on the circular scale corresponding to a thickness of 0. to line the orbital cavity after exenteration or as a cover for a floor of mouth or tongue raw surface. A thicker graft of 0. placed in a sterile pot and refrigerated at 4°C. it be placed keratin side down on tulle gras. The length of the flap corresponds to the area supplied by these vessels. which may still occasionally be used to replace lateral . (b) To cover excised conchal bowl skin and cartilage defect after the excision of a basal cell carcinoma. When planning such a flap the length of the flap should not exceed the width of the base otherwise the distal portion of the flap may become ischaemic. Where possible. It is recommended that. the use of relaxed skin tension lines should be used. This consists of the epidermis and the whole of the dermis. The donor site should be hairless and inconspicuous. careful planning is necessary to obtain optimal cosmesis. axial and myocutaneous. Although these flaps may be raised anywhere and run in any direction. Axial. advancement. Random. (c) To line cavities. Unroll the graft onto the donor site after 3–5 days when all bleeding and serous ooze from the raw bed has stopped and vascular granulated tissue has started to form. rotation or transposition skin flaps.RECONSTRUCTIVE SURGERY 269 promptly dispersed by making a small nick in the graft and drawing out the collection using a sterile cotton bud. Level 3 Pedicled skin flaps.4 mm. Skin gets its blood supply either from direct cutaneous vessels which run superficial to the deep fascia or from indirect vessels which pass from feeding vessels through muscle or fascia to reach the skin. Full-thickness skin graft (Wolfe graft). The inner aspect of the upper arm or thigh is therefore recommended. after taking the graft at operation. which is rolled. Split skin grafts consist of epidermis and a thin layer of dermis. The postauricular donor site is preferred because primary closure is easy and leaves an inconspicuous scar. These are skin flaps that remain attached at their base to provide a blood supply and lymphatic drainage. Indications (a) Nasal tip and conchal bowl defects. for example radial forearm free flaps and deltopectoral flaps. for example the inner layer of a maxillectomy cheek flap. Indications (a) To cover donor sites. Split skin grafts.

A pectoralis major flap is an example. the pectoralis major flap is now by far the most popular. This flap is based on the inferior epigastric vessels. Its advantages are that it is straightforward to raise. (d) Rectus abdominis myocutaneous free flap. A take rate of at least 90% should be obtained. the second to return the pedicle to its original site after the distal portion has gained an adequate blood supply at its new site. (b) after measuring the flap allow an extra 1–2 cm of pedicle length as the flap retracts on raising. Reconstruction of a neopharynx after pharyngolaryngectomy. Between stages the patient must endure moist dressings to an unsightly granulating bed from which the flap has been lifted. and for this reason the radial forearm fasciocutaneous free flap has taken over much of its previous work. Common free tissue transfer flaps in head and neck reconstruction with their main indications are: (a) Radial forearm fasciocutaneous free flap. The osseous portion of this free flap is very reliable but the skin less so. The length available depends on the interval between the insertions of pronator teres and pronator quadratus. The vessels perforate the muscle to supply the overlying skin. (c) Composite osteocutanous radial forearm free flap. Reconstruction of mandibulectomy greater than 8–10 cm. Raising the flap and preparing both the donor and recipient vessels and their subsequent anastomosis are critical areas in which small errors may cause the graft to fail. Reconstruction of the floor of mouth and mandible after a mandibulectomy of less than about 8–10 cm. (e) Iliac crest osteocutaneous free flap based on the deep circumflex iliac vessels. One should aim to take no more than 40% of the diameter of the radius in the composite flap in order to reduce the risk of a subsequent radial fracture. Reconstruction following total glossectomy and reconstructing the lateral skull base after petrosectomy. soft palate and the repair of a pharyngocutaneous fistula. Good results come from expert training in a centre with an interest in such reconstructive surgery and cannot be learned from a book. Musculocutaneous. Two important points in technique in raising the flap are: (a) suture the muscle edge to the subcutaneous edge as the flap is raised to prevent shearing of the perforating vessels. provides good bulk and is reliable. The main disadvantage of these flaps is that the patient must submit to a twostage procedure. in particular a hemimandibulectomy with or without floor of mouth reconstruction. It runs in a layer between the deep aspect of the muscle and its underlying fascia. Level 4 Free tissue transfer. Its main disadvantage is that its bulk may compromise function. These flaps provide the gold standard in terms of cosmesis and preservation of function. Although a large number of head and neck musculocutaneous flaps have been described. deep fascia and muscle based on the acromiothoracic artery. tongue. .270 OTOLARYNGOLOGY neck skin and peristomal skin. This is a flap of skin. it is important that the pedicle is not under tension when suturing the flap into position. a branch of the first part of the axillary artery. Reconstruction of the floor of mouth. Good results require sound microvascular training and meticulous attention to detail. this normally takes 3–4 weeks. (b) Jejunal free flap. lateral oropharyngeal wall.

p. Oropharyngeal carcinoma. 70–91. Related topics of interest Hypopharyngeal carcinoma. p. 203. London: Baillière Tindall. In: Shaheen OH (ed). . 124. p.RECONSTRUCTIVE SURGERY 271 Further reading Shaheen OH. The repair of defects. 1984. Problems in Head and Neck Surgery. Oral cavity carcinoma. 197.

The salivary glands are affected in approximately 40% of all cases. Infection. cirrhosis. In one in six patients the disease will progress to a lymphoma. Coproxamol (dextropropoxyphene and paracetamol).SALIVARY GLAND DISEASES There are four main salivary glands—two parotids and two submandibular glands—and multiple minor salivary glands which occur throughout the upper respiratory tract. bulimia. thiouracil. 4. Metabolic. Sjögren originally described xerostomia. 3. Non-epithelial: haemangioma. Sjögren’s syndrome is an autoimmune disease which is characterized by periductal lymphocytes in multiple organs. . 5. which consists of xerostomia. leprosy. Drug induced. neurofibroma. (b) Secondary Sjögren’s syndrome. with no mention of salivary gland swelling. actinomycosis. notably in the oral cavity and oropharynx. Malignant: adenoid cystic carcinoma. alcoholism. Cushing’s disease. (b) Bacterial: staphylococcal. tuberculosis. oral contraceptive pill. 2. Pathology 1. xerophthalmia and a connective tissue disorder. keratoconjunctivitis sicca and rheumatoid arthritis. (a) Viral: mumps virus. lymphoma. coxsackie virus. acinic cell tumour. usually rheumatoid arthritis. Now the disease can be classified into: (a) Primary Sjögren’s syndrome (or sicca complex) consisting of xerostomia and xerophthalmia with no connective tissue component. echovirus. Neoplasm. adenolymphoma. lymphangioma. human immunodeficiency virus (HIV). Patients with enlargement of these glands or sialomegaly can pose an interesting diagnostic dilemma. diabetes. isoprenaline. gout. adenocarcinoma. squamous cell carcinoma. (a) (b) (c) (d) Benign: pleomorphic adenoma. Myxoedema. phenylbutazone. Inflammatory. Variable: mucoepidermoid carcinoma.

Sialectasis. Tests for the relevant endocrine disorders may be appropriate. These disorders should be kept in mind as they may mimic sialomegaly: hypertrophic masseter. A . Before palpating the lesion be sure to ask if it is tender. The history should include the age of the patient (think of mumps or congenital sialectasis). Radiography. Then examine the pharynx to look for a parapharyngeal lesion (in particular one arising from the deep lobe of the parotid). The social history including alcohol intake and risk of HIV infection may be relevant in some cases. MRI scanning is usually the preferred investigation in neoplastic disease to delineate any potential deep lobe involvement and to assess the tumour’s relationship to the facial nerve. dental cyst. winged mandible. There should be a thorough review of systemic symptoms (metabolic causes). but the results have to be interpreted in conjunction with clinical suspicion as incorrect reports are not uncommon. Inflamed skin over the swelling should make one consider an infection or skin involvement from a malignant lesion. Progressive destruction of the alveoli and parenchyma of the gland accompanied by duct stenosis and cyst formation. Many cases are thought to be congenital. which may push the tonsil medially. Investigations 1. calculi and sialectasis can all be diagnosed if sialography is possible. 7. In the floor of the mouth a submandibular calculus may be felt or pressure on a parotid gland may express pus from the parotid duct. Inspect the oral cavity and palpate all of the glands bimanually. Rheumatoid factor. sebaceous cyst. Duct stenosis. Blood tests. The facial nerve should be tested as facial weakness also raises the suspicion of a malignant lesion.SALIVARY GLAND DISEASES 273 6. this is kind to the patient and a good habit in clinical medicine—it is essential in an examination! Palpation should determine whether the lesion is local or diffuse. Incisional and Trucut biopsy should not be performed as there is a risk of seeding neoplastic disease. solid or cystic. Most submandibular gland calculi are radiopaque. and any medication the patient is taking should be noted. Complete the ENT examination and perform a general examination if systemic or disseminated neoplastic disease is suspected. Specific Sjögren’s antibodies are usually also present (SSrho and SSla). mandible tumours. duration of symptoms (benign tumours grow slowly and malignant ones fairly rapidly) and any related pain (infection. branchial cyst. antinuclear factor and abnormal electro-phoresis are sometimes found in Sjögren’s syndrome. lipoma and neuroma of the facial nerve. Epithelial debris or calculi may be found in the main ducts. 2. but most parotid calculi are radiolucent. Biopsy. the number of glands affected (tumours are unilateral apart from Warthin’s on rare occasions). especially with cystic lesions. Fine-needle aspiration biopsy is safe and often useful. Examination Inspect the enlarged gland and then all the other salivary glands. History The diagnosis is often obvious from the clinical findings. calculus or adenoid cystic carcinoma). A sialogram is probably the most useful investigation of benign salivary gland disease. 3. whether the swelling is exacerbated by eating (calculus disease secondary to sialectasis). A plain film is useful as it may reveal a radiopaque submandibular calculus. preauricular lymph node. mobile or fixed and whether or not other glands are affected. Pseudoparotomegaly.

274. Non-neoplastic salivary gland disease.274 OTOLARYNGOLOGY parapharyngeal mass should never be biopsied through the pharynx because there may be uncontrollable bleeding if the patient has a vascular lesion. 1997. In: Scott-Brown’s Otolaryngology. 6th edn. Sublabial biopsy is the definitive investigation to confirm the diagnosis in Sjögren’s syndrome (periducatal lymphocytic infiltration found). 5. p. Further reading Maran AGD. Management The management and specific treatment of the patient depends on the cause of the salivary gland swelling. chapter 19. London: Butterworth. Vol. Related topic of interest Salivary gland neoplasms. .

In addition. if one can remember the epithelial and the non-epithelial histology of the organ. acinic cell carcinoma. Haemangioma. extension to the deep lobe and relation to the facial nerve. Using . Clinical assessment All patients with a mass in a salivary gland should have: an inspection and palpation of the mass itself. peroral palpation. 2. A good approximation to remember is that 80% of all salivary tumours are in the parotid. Benign. and malignant lesions can be primary or secondary. oral examination with particular inspection of the relevant salivary gland duct.SALIVARY GLAND NEOPLASMS Pathology Neoplastic lesions are divided into benign or malignant. A simplified classification is presented below: 1. Investigations 1. Warthin’s tumour (papillary cystadenoma lymphomatosum). facial nerve assessment and neck node palpation. Adenoid cystic carcinoma. carcinoma expleomorphic adenoma. neurofibroma. lymphoma. oncocytic adenoma. undifferentiated carcinoma. 3. Malignant. an excellent framework for working practice is easily established. inspection of the oropharynx for parapharyngeal extension assessment. except that some such neoplasms have variable biological behaviour. 4. CT scanning of a parotid tumour is useful in the assessment and delineation of anatomical structures.g. Variable. Classification The WHO histological classification of salivary tumours now includes over 35 variants and also includes tumour-like lesions (e. squamous cell carcinoma. Pleomorphic adenoma. Mucoepidermoid carcinoma. adenocarcinoma. ductal papilloma. salivary gland cysts). lymphangioma. Non-epithelial. Radiography. monomorphic adenoma. Salivary gland tumours are no exception in this respect. One in three tumours arising in the submandibular gland and one in two tumours that arise in the minor salivary glands are malignant. MRI has significant advantages. 80% of parotid tumours are benign and 80% of the benign tumours that arise in the parotid are pleomorphic adenoma.

2. Microscopically it comprises epithelial and mesodermal elements with a mucopolysaccharide stroma giving rise to a characteristic mixed staining pattern. soft tissues). The role of FNA in the diagnosis of benign and malignant salivary gland disease is a controversial issue. It has a pseudocapsule of compressed parotid tissue into which the tumour usually has many protuberances. Benign tumours 1. Ten per cent are bilateral. a significant correlation exists between tumour stage and survival. rarely radical surgery is needed with resection of the facial nerve. It arises from intercalated duct cells and myoepithelial cells. A tumour of any size with significant local extension.276 OTOLARYNGOLOGY STIR sequencing appears to add to the sensitivity in detecting lesions of the parotid gland. If the result of FNA is at variance with other findings then clinical judgement should prevail. which is almost invariably hypocellular or acellular. They are soft and cystic tumours which are thought to arise from heterotopic parotid tissue in the lymph nodes within the parotid gland. but rarely synchronously. recurrence almost never occurs. without extraparenchymal extension (skin. Proponents of the technique argue that FNA provides diagnostic information which may allay a patient’s anxiety and aid in preoperative counselling and planning of surgery. FNA is a relatively painless procedure. > 6 cm in diameter. those against the routine use of FNA argue that one cannot rely on the sensitivity or specificity of the procedure. 2. Management of recurrent tumour is difficult as the facial nerve may be involved and its sheath may need to be stripped. Fine-needle aspiration biopsy (FNA). unlike pleomorphic adenoma. Superficial parotidectomy or hemisuperficial parotidectomy when the lesion is small is now the preferred procedure. 2–4 cm in diameter. and thus non-diagnostic. However. delineating the facial nerve and in identifying the tumour edge. The UICC system is summarized below: T0 T1 T2 T3 T4a T4b No clinical evidence of tumour. Treatment is by excision and. The sex distribution is equal and the peak age incidence is in the fifth decade. Pleomorphic adenoma is the commonest benign salivary tumour. < 2 cm in diameter. The facial nerve should if at all feasible not be sacrificed. Staging With malignant tumours of the parotid gland. causing recurrence. Warthin’s ‘s tumour (papillary cystadenoma) is a benign tumour. usually seen in elderly men. Monomorphic adenomas arise from ductal epithelium and are treated by surgical excision with a cuff of tissue. then tumour may implant. Many surgeons advocate adjuvant postoperative radio-therapy in these situations. If the capsule is ruptured during removal. . They are therefore excised with as large a margin as possible to reduce the risk of capsule rupture. without extraparenchymal extension. 3. in whom the aspirates often yield straw-coloured fluid. has few complications (seeding of the tumour does not appear to occur) and may prevent an ill-advised and often ill-fated incisional or excisional biopsy of a parotid mass. and/or base of skull or facial nerve invasion. and/or extraparenchymal extension (but not facial nerve). The stage of the disease has been shown to be a more important prognostic parameter than its histological grade. The peak incidence is the seventh decade and the male-female ratio is 7:1. This is particularly true in patients with cystic lesions of the parotid. 4–6 cm in diameter.

Second Consensus. The sex incidence is equal and they are seen most often in patients in their sixth decade. Malignant tumours 1. it is often involved. intermediate ones are more aggressive and high-grade or undifferentiated tumours metastasize early and carry a poor prognosis. Caslin AC. However. however. 2000. 107:1025–1028. Current Opinion in Otolaryngology and Head and Neck Surgery. Adenocarcinoma accounts for about 3% of parotid tumours and 10% of submandibular and minor salivary gland tumours. Tumours with variable behaviour 1. Journal of Laryngology and Otology. 271. Effective Head and Neck Cancer Management. 3. and in this situation it needs wide excision and anastomosis with a nerve graft. Head and Neck Surgeons. Further reading Medina JE. Radiotherapy in the curative and palliative treatment of patients with adenoid cystic carcinoma of salivary gland origin is useful in some cases. Mucoepidermoid carcinoma arises in any salivary tissue but predominantly the parotid gland. The incidence of lymph node metastases is low and distant metastases occur late. Acinic cell carcinoma is similarly difficult to classify. Low-grade or well-differentiated tumours usually behave in a benign fashion. 2. Wilson J (ed). The tumour is slow-growing and tends to spread along nerve sheaths.SALIVARY GLAND NEOPLASMS 277 4. but is more common in minor than in major salivary glands. It is usually found in the superficial lobe of the parotid. If the facial nerve is free of tumour it may be dissected out and left intact. the behaviour is not always accurately predicted by the histological appearance. The patients often complain of facial pain and may present with a facial paresis. regarding them as high-grade mucoepidermoid tumours. Squamous cell carcinoma. Jones AS. They are. much more benign than mucoepidermoid tumours. true malignant pleomorphic adenomas are rare. Some pathologists doubt their existence. p. but is still being assessed. Oncocytoma is a benign eosinophilic tumour (also called oxyphil adenoma) that arises from intralobular ducts or acini. However. 1993. Fine needle aspiration cytology of salivary gland lesions reported immediately in a head and neck clinic. Postoperative radiotherapy will not affect the graft. Treatment is usually by radical excision and adjuvant radiotherapy. It is the commonest salivary neoplasm in children. Related topic of interest Salivary gland diseases. . Salivary gland tumours. 2. Roland NJ. 1: 91–96. The sural nerve is preferred as the greater auricular nerve may be involved and should also be excised. British Association of Otolaryngologists. Adenoid cystic carcinoma is the commonest malignant tumour and may arise from any salivary tissue. It can undergo malignant change and treatment is also by excision with a cuff of tissue. 1993.

Aetiology 1. Inhalation of irritants. latrogenic (SMR. Trauma. A very small perforation may cause whistling on nasal breathing. Inflammatory (Wegener’s granulomatosis. Septal perforations are usually preceded by ulceration except when following a septal haematoma or septal abscess.SEPTAL PERFORATION Perforation of the nasal septum is most common in the anterior cartilaginous part except for that caused by syphilis. 2. Occupational (hexavalent. Drugs (cocaine. sport injury). In any patient where there is uncertainty about the cause. Idiopathic. septoplasty. adenocarcinoma. 5. The main complaints are recurrent epistaxis. Injury (assault. basal cell carcinoma. usually as a complication of septal surgery. snuff). tuberculosis). alkaline dusts). T-cell lymphoma). Clinical features The majority of perforations are asymptomatic. Neoplasm (Squamous cell carcinoma. 6. systemic lupus. nasal cautery). 3. arsenic. Infection (Syphilis. the worse the symptoms. the following tests should be performed: . crusting and nasal obstruction. The larger the perforation and the more anterior its position. polyarteritis nodosa. Many septal perforations that were previously considered to be idiopathic are now thought to be secondary to nose picking. The severity of the symptoms depends on the position and the size of the perforation. chrome. Most perforations are iatrogenic in origin. chronic relapsing polychondritis). Self-inflicted (nose picking). road accident. Investigations The history will very often give the diagnosis. dryness in the nose. 4. which normally involves the bony septum. particularly when the Killian incision is used.

Bull TR (eds). the severity of the symptoms and the particular treatment the patient has been given. Scott-Brown’s Otolaryngology.SEPTAL PERFORATION 279 • Blood tests should include an FBC. A variety of operations including the use of split-skin grafts. Silver nitrate cautery can be applied to bleeding granulations. Medical treatment with 25% glucose in glycerol drops will loosen and help clear crusts. A patient with a silastic button should be seen at regular 4–6-monthly intervals to decrust and clean the prosthesis. Vol. The nasal septum. Follow-up and aftercare This will depend on the cause of the perforation. p. • A biopsy from the edge of the perforation if there is suggestion of a neoplasm or granuloma. buccal mucosa or sublabial myomucosal flaps. If the perforation continues to trouble the patient it is worth trying to plug the hole with a silastic septal button. septal mucoperichondrial flaps. Related topic of interest Nasal trauma. Wegener’s granulomatosis or metastases. ESR. 4. London: Butterworth. Paradoxically. Treatment The first objective is to cure the causative disease process before specific treatment of the perforation. FTA for syphilis. 177. 1997. Barrier creams can help prevent drying and crusting. • A chest radiograph may show lesions in tuberculosis. Surgical closure of the perforation is difficult to achieve. • Urinalysis (haematuria or proteinuria may result from nephritis in Wegener’s granulomatosis or polyarteritis). perforations that cause a whistle can be treated by enlarging them. Treatment is usually indicated when there is troublesome crusting or bleeding. Many perforations are asymptomatic and informed reassurance is all that is required. composite grafts from the pinna and moving septal cartilage to fill the hole have all been described. Further reading Brain D. In: Mackay IS. 6th edn. . ANCA for Wegners.

Epithelial (papilloma. and smoking cigarettes have recently been implicated as providing an increased risk of squamous cell carcinoma. a quarter from the ethmoids and a quarter from the nasal cavity. 10% lymphomas and about 4% adenocarcinomas. chordoma. Benign. Non-epithelial (fibroma. adenoma and inverted papilloma). Pathology About 10% of head and neck cancer is sinonasal with an incidence in the UK and the USA of about 10 per million. 2. Histologically 50% are squamous cell carcinoma. The association between the ethmoidal adenocarcinoma and hardwood workers is well documented. the Japanese and Africans. meningioma and osteoma). haemangiopericytoma. odontogenic. . Malignant Epithelial (squamous cell carcinoma. malignant melanoma. anaplastic carcinoma. The male: female ratio in series varies between 1:2 and 1:5. adenocarcinoma. 15% anaplastic. Chronic nasal pathology. Schwannoma. It is about double this in Arabs. chondroma. Their low incidence and the lack of a consensus regarding staging has made comparison of treatment regimes between centres difficult. 1. including sepsis and Wegener’s granulomatosis. and fibroosseous tumours. Workers handling chromate salts and those involved in nickel refining are at an increased risk of nasal malignancy. transitional cell carcinoma. Immunocytochemical analysis (in particular neurone specific enolase) of the small cell cancers (anaplastic and lymphomas) will reveal a proportion to be olfactory neuroblastomas. salivary gland malignancy in particular adenoid cystic carcinoma and olfactory neuroblastoma. non epithelial. Human papilloma virus genome has been identified and therefore implicated as an aetiological agent in non-dysplastic and dysplastic inverted papilloma and squamous cell carcinoma. Classification Both benign and malignant groups can be classified into epithelial. nasal glioma. The latter constitute a considerable challenge to the head and neck surgeon as they often present with advanced disease.SINONASAL TUMOURS Tumours of the sinonasal region comprise a diverse group of benign and malignant neoplasms. haemangioma. Half of sinonasal cancer arises from the upper jaw.

Further delays may arise because these symptoms are not usually associated with carcinoma by primary care physicians. High grade T cell lymphoma (formerly lethal midline granuloma): see Related topic Non-healing nasal granulomata. Microscopically there are deep invaginations of epithelium into the stroma.SINONASAL TUMOURS 281 Non-epithelial (fibrosarcoma. Frontoethmoidal and antral malignant melanoma have a much worse prognosis. where the prognosis is reasonable. It always involves the cribriform plate so if resection is contemplated this must be via a craniofacial approach. nasal cavity and anterior cranial fossa. Cheek swelling occurs only when the tumour has breached the anterior antral wall to impinge on periosteum. This indicates a poor prognosis but not necessarily incurability. . There is no relationship between Clark’s classification (penetration of specific skin layers) and prognosis in this region although the latter is associated with Breslow’s classification (thickness of the lesion in mm). Five per cent of subjects will have a metastatic neck lymph node. Probably less than 2% undergo malignant change although there may be a synchronous sinonasal squamous cell carcinoma in up to a further 10%. rhabdomyosarcoma. A quarter of patients will die from distant metastases. Important benign sinonasal tumours Inverted papilloma. with microcyst formation. Malignant sinonasal tumours Squamous cell carcinoma and adenocarcinoma both usually present at an advanced stage because their presenting symptoms of epistaxis. Osteomas most commonly arise from the frontal region where they may expand medially to block the frontal recess predisposing to a secondary mucocele or frontal sinusitis. It is usually impossible to define a site of origin of the carcinoma due to its diffuse extent. It arises from neural crest stem cells. is the most important of this group forming about 5% of all nasal tumours. The epithelium retains its basement membrane. angiosarcoma. chondrosarcoma. usually upper deep cervical. and osteogenic sarcomas). is not usually detectable. superiorly where they may erode the cribriform plate or posteriorly to erode the posterior wall of the frontal sinus and impinge on frontal lobe dura. and microscopically resembles other small cell malignancies such as high grade lymphoma and anaplastic carcinoma. Adenoid cystic carcinoma is particularly difficult to eradicate because of its ability to spread via the branches of the trigeminal and olfactory nerves along perineurium. Macroscopically there is usually a papilliferous exophytic mass. on presentation. inferiorly to displace the orbit. orbit. They consist of hard cortical bone and require excision if symptomatic or enlarging. Olfactory neuroblastomas were undoubtedly under reported until recently when immunocytochemical stains for this tumour became available. This may include the cheek. with a propensity to recur many years after apparent cure. nasal obstruction and headaches occur only with a significant tumour mass. the precursors of olfactory cells. most commonly the bronchus. This emphasizes the need for careful nasendoscopic follow up. Haemangiopericytomas may arise anywhere in the sinonasal region and have a spectrum of aggression. All ages are affected and urine vanillylmandelic acid (VMA). Malignant melanomas comprise 1% of sinonasal carcinomas and usually arise from the septum or lateral nasal wall. originally described by Ringertz.

trismus and ethmoidal symptoms occur with advanced disease. Bone does not generate a signal. Epistaxis. 3. involving sphenoid and/or frontal sinus and/or skin of nose. Nasendoscopy may reveal tumour extruding from the middle meatus. T1 T2 T3 T4 Tumour confined to ethmoid with or without bone erosion. A T2 weighted or STIR sequence MRI scan may distinguish tumour from inflammation. Carcinoma in situ. Features are similar to frontal osteomas except the history is shorter and more rapidly progressive. Epistaxis. T1 Tumour limited to the antral mucosa with no erosion or destruction of bone.282 OTOLARYNGOLOGY Staging The UICC staging is as follows: Tx T0 Tis Primary tumour cannot be assessed. T4 Tumour invades orbital contents beyond the floor or medial wall including apex and/or any of the following: cribriform plate. nasal obstruction and a mass visible on nasendoscopy. Antral. nasopharynx.. Nasal cavity tumours. skin of cheek. including extension into the hard palate and/or middle nasal meatus. nasal obstruction and if the lamina papyracea is breached. base of skull. headache if blocking the osteomeatal complex and atypical facial pain (suggesting involvement of the pterygopalatine fossa or the infra orbital nerve). Tumour with intracranial extension. Epistaxis. T3 Tumour invades any of the following: bone of posterior wall of maxillary sinus. T2 Tumour causing bone erosion or destruction. Investigations A high definition CT scan on both bone and soft tissue windows is the ideal to show soft tissue and bone involvement. orbital extension including apex. except for the posterior wall. . Ethmoid sinus. Oroantral fistula. 4. floor of medial wall of orbit. Clinical features 1. nasal obstruction. sphenoid sinus. epiphora and diplopia. retained secretions and fat. Frontal sinus. ill-fitting dentures. cheek swelling. Ethmoidal. Maxillary sinus. subcutaneous tissues. Tumour extends into nasal cavity. Tumour extends to anterior orbit and/or maxillary sinus. No evidence of primary disease. frontal sinus. proptosis. 2.

In general an orbital exenteration is indicated only if tumour breaches periostium to involve orbital fat. Limitations of the endoscopic approach include tumour extending into the frontal sinus and anterior wall of maxilla. quarterly for the third and six-monthly until five years post surgery. bimonthly for the second. Those who have a lateral rhinotomy or craniofacial cavity often have excessive crusting in the early post-operative phase. Tumour limited to the anterior ethmoids or isolated middle turbinate or middle meatal lesion are ideal for endoscopic resection. (b) Total maxillectomy. Overall a five-year survival of 40–50% would be reasonable. Some surgeons thereafter review annually for a further five years. Carcinoma. well fitting and easily removable obturator. An upper limb extension will allow tumour limited to the frontal ethmoidal region to be accessed. Free flaps or a temporalis muscle swing flap will fill in the cavity and produce the optimum cosmetic result. Adjuvant radiotherapy may be indicated depending on tissue margins. 2. . Draf quotes a recurrence rate of 9% by the endoscopic approach. It prevents an external scar. Inverted papilloma. Glycerine and glucose nose drops and regular douching with saline will minimize this. comfortable. Recent studies have demonstrated recurrence rates no higher than with external approach surgery. There are three main surgical options for carcinoma: (a) Lateral rhinotomy for tumour limited to the lateral nasal wall. For antral carcinoma. but have the disadvantage that they may mask an early recurrence. The technique allows direct visualization of tumour and its extent can be accurately identified during surgery. (c) Craniofacial resection is indicated when the cribriform plate is involved or breached.SINONASAL TUMOURS 283 Treatment 1. Extensive experience and a high level of expertise in endoscopic sinus surgery is a prerequisite to undertaking the endoscopic approach. In essence provided the endoscope can visualize the distal extent of tumour during surgery then endoscopic resection is a reasonable and perhaps preferred alternative to external approach surgery. Reconstruction is by primary closure where possible. Further review allows a fine tuning of the prosthesis to provide a light. Prognosis by stage is difficult for reasons already outlined. there is less blood loss and the hospital stay is shorter. nasal cavity and ethmoid. There is significantly less morbidity by the endoscopic approach. Split thickness skin grafts should line the exenteration cavity. Recent work has also shown its application for tumours involving the posterior ethmoids and anterior wall of sphenoid. laryngopharyngeal examination to exclude a second primary and neck examination to look for metastases should be monthly for the first post-operative year. Only the surgeon should extract crusts from the nares of the craniofacial patient as these may be attached to a fascia lata or temporalis fascia graft overlying the anterior cranial fossa. Follow-up which involves nasendoscopy to inspect the surgical cavity created or direct inspection of a maxillectomy cavity after obturator removal. The accurate identification of disease extent with CT and MRI imaging has allowed the advent of endoscopic resection for inverted papilloma. Wigand’s figures for disease of similar extent are 17% recurrence rate for the endoscopic approach and 19% for external approach surgery at 2 years followup. Follow-up and aftercare Ideally an orthodontist should take an impression of the maxillectomy cavity at operation in order to make a temporary obturator. Post-operatively endoscopic inspection of the surgical cavity allows accurate monitoring of patient progress and early identification of recurrence.

Current Opinion in Otolaryngology and Head and Neck Surgery. Brors D and Draf W. 170. 2000. 1988. Related topic of interest Nasal granuloma. Wilson J (ed). Harrison DFN. 156:187–190. 11:279–283. 1999. 1989. Cheesman AD. Effective Head and Neck Cancer Management. Donald PJ. 5: 73–78. p. 1997. Howard DJ. . Management of sinus malignancy.284 OTOLARYNGOLOGY Further reading Lund VJ. Head and Neck Surgery. American Journal of Surgery. The treatment of inverted papilloma. Head and Neck Surgeons. Magnetic resonance imaging of paranasal sinus tumors for craniofacial resection. Lund VJ. British Association of Otolaryngologists. Craniofacial resection for tumors of the nasal cavity and paranasal sinuses. Lloyd GAS. Current Opinion in Otolaryngol and Head and Neck Surgery. 7:33–39. Second Consensus.

tobacco smoke). Any condition narrowing or blocking these may lead to secretion retention and poor ventilation. followed by the ethmoid. • Nasal anatomical variations (septal deviation.e. • Fractures involving the sinuses. General. • Upper respiratory tract infection (acute infective rhinitis. Immunocompromised host. 1. • Nasal polyps. • Dental extraction or infection (diseases of the upper premolars and molars). fumes. • Swimming and diving. Atmospheric irritants (dust. Both the maxillary and frontal sinuses drain through narrow spaces and interstices into the middle meatus. The ethmoids also drain into this and the superior meatus. • Nasal foreign body. • Nasal tumour. etc). i. • • • • Debilitation. Acute sinusitis Acute inflammation of one or all the sinuses may occur (pansinusitis). Local. The maxillary sinus is clinically the most commonly affected. • Pre-existing rhinitis (allergic.SINUSITIS Predisposing factors The commonest causes are nasal. abnormal uncinate process. Kartagener’s syndrome. 2. tonsillitis or adenoiditis). vasomotor. frontal and sphenoid sinuses in that order. cystic fibrosis). thus predisposing to consequent infection.g. rhinitis medicamentosa. middle turbinate or ethmoid bulla) narrow the infundibulum and predispose to its occlusion when there is intercurrent disease. Mucociliary disorders (e. common cold or influenza. .

Percussion over the upper teeth may elicit tenderness. . The fullness in the face and pain may be exacerbated by bending forward or stooping down.286 OTOLARYNGOLOGY Pathology The majority of cases follow a viral upper respiratory tract infection which involves all of the respiratory epithelium including the paranasal sinuses. and Staphylococcus aureus. Haemophilus influenzae (pneumococcal and haemophilus infections accounting for 70% of cases in adults). Where possible pus from the nose should be cultured and blood cultures should be taken if there is systemic upset. Herpes zoster. Moraxella catarrhalis. fullness in the face. ideally using both soft-tissue and bone window settings. Frontal sinusitis produces pain in the forehead and tenderness below the eyebrows. leading to stasis of secretions predisposing to secondary bacterial infection. Klebsiella pneumoniae. which blocks the ostia. Sinonasal tumour. The usual causative organisms are Streptococcus pneumoniae. malaise and possibly a pyrexia. Radiological investigation may show an opacity or fluid level. Ethmoid sinusitis may cause pain between the eyes accompanied by frontal headache. Pain developing in the cheek or upper teeth indicates maxillary sinus involvement. Such infections cause hyperaemia and oedema of the mucosa. Trigeminal neuralgia. Clinical features The symptoms usually occur several days after developing an upper respiratory tract infection. The patient will have pain over the infected sinus. Temporal arteritis. Sphenoid infection may produce retro-orbital pain. Anterior rhinoscopy may show red oedematous nasal mucosa and turbinates. suggesting a dental origin of maxillary sinusitis. There will be cellular infiltration and an increase in mucus production. although plain X-rays are rarely if ever used (see Radiology). Specific features may indicate the sinus that is infected. Endoscopy with a 0° or 30° scope may reveal pus in the middle meatus or sphenoethmoidal recess. Dental pain. or pain anywhere across the vault. but may develop in immunocompromised or elderly diabetic patients. Escherichia coli and Streptococcus faecalis may spread from a dental source. Investigations An elevated white cell count and erythrocyte sedimentation rate (ESR) will confirm an acute infection. nasal congestion. Erysipelas. Differential diagnosis • • • • • • • Migraine. It may also be possible to elicit tenderness over the infected sinus. When there is doubt about the diagnosis. Acute fungal infections (for example mucormycosis and aspergillosis) are rare. Streptococcus pyogenes. The infection will also paralyse the cilia. further confirmation can be obtained by a high-definition coronal CT scan.

It can be given locally or systemically. The decongestant may reduce nasal oedema. postnasal drainage. Pathology There is an increase in vascularity and vascular permeability. 1. Multiple small abscesses occur in the thickened mucosa and fibrosis of the submucosal stroma supervenes. Surgical treatment. cefuroxime) is recommended for penicillinresistant pneumococci. to prevent complications and to correct any precipitating factor. The patient should be reviewed after resolution of the acute phase. Any pus obtained should be cultured. Frontal sinu-sitis which does not respond to these measures may requires trephine of the floor of the sinus via a small incision above the medial canthus.g. This is best performed with the aid of an endoscope. Functional endoscopic sinus surgery (see p.g. diet. clarithromycin). Figures from the USA however. This will not only treat any infection in the maxillary sinus but will also promote drainage from the other sinuses. septoplasty for septal deviation) should be organized. 108) is now considered to be the treatment of choice. the incidence of sinusitis has increased. hygiene. The patient should have a full 7-day course of the antibiotic. There is no consensus view on what constitutes chronic sinusitis. and aid infundibular drainage. co-amoxyclav. facial pain) and signs (CT.SINUSITIS 287 Management The aims of treatment are to resolve and limit the course of the acute infection. and hopefully open the natural ostia of the sinuses to allow free drainage. Ulceration of the epithelium will result in the formation of granulation tissue.g. It has been stated that the incidence of this problem in the UK has been reduced by improvements in the general health of the population. It may be necessary to perform repeat antral washouts for some patients. The ethmoid sinuses can be uncapped to promote drainage if they are specifically diseased and an anterior sphenoidotomy may be necessary for acute sphenoiditis. • A decongestant (e.g. Those surgeons who follow the philosophy of functional endoscopic sinus surgery claim that if definitive endoscopic sinus surgery is performed in the acute phase no further washout should be necessary. The changes in the mucosa over . by placing a pledget of cocainized cotton wool into the middle meatus for 20 minutes. It is usually considered to be a condition in which sinusitis symptoms (congestion. Chronic sinusitis accounts for over 85% of all clinic visits for sinusitis in adults. paracetamol). If acute sinusitis fails to respond to medical treatment. then the patient may need antral puncture and washout.g. This leads to oedema and hypertrophy of the mucosa which may become polypoidal. If the patient has suffered recurrent infections it may be appropriate to perform an intranasal antrostomy for better and longer-lasting drainage. Goblet cell hyperplasia and a chronic cellular infiltrate will occur. Medical treatment In the acute stages the patient should have: • Bed rest and adequate simple analgesia (e. but in some cases the onset is more insidious. and the introduction of antibiotics. Chronic sinusitis Chronic inflammation of the sinuses usually follows recurrent acute sinusitis. confirm that over the past decade. A second generation cephalosporin (e. nasal discharge. The current practice of many rhinologists is to shrink the mucosal lining. Correction of any obvious precipitating factor (e. 2. pseudoephedrine or xylometa-zoline). endoscopy) persist for weeks to months. • Broad-spectrum antibiotic (e.

antihistamines. often when it is not. temporomandibular joint diseases. Plain sinus radiographs are rarely indicated now because they may show varying degrees of opacification of the involved sinuses with mucosal thickening. should be treated with medical therapy (e. optic nerve or dura is less likely. such as inflammatory disease. nasal or postnasal discharge and pain. Furthermore. A course of broad-spectrum antibiotics in combination with a decongestant should be tried initially (though they should be avoided long-term). especially in infections of dental origin. Step-wise removal of the ethmoidal cells extending to the posterior ethmoid and sphenoid sinus . some patients with sinogenic headaches may present with an atypical history and have negative findings on examination and plain sinus radiographs. barotrauma or another readily identifiable cause. (c) Those whose problems are not clear and in whom there seems to be no overt indication of sinus disease.g. A headache over the forehead. It has been suggested that chronic paranasal sinus pain alone should not constitute chronic sinusitis. to ventilate the sinus and to restore normal mucosal lining in the sinus. oral course of steroids). the bridge of the nose and the face is common. 1. (b) Those with headaches clearly traceable to non-sinus causes such as migraine. Medical. This does not rule out a sinus cause for their problem. The principal aims of treatment are to correct the predisposing cause. The definition of chronic sinusitis becomes important in comparing studies on the disease. One modality is said to enhance the accuracy of the other. Investigations Only the combination of diagnostic endoscopy and high-definition coronal section CT scanning will provide the maximum information. glaucoma. because different patient inclusion criteria may affect study results. The ENT surgeon is confronted as a rule with three different groups of headache patients: (a) Those with headaches clearly connected to a sinus problem. Those who advocate this procedure claim that more accurate surgery can now be undertaken and that injury to the eye. Differential diagnosis It is not uncommon for general practitioners and those in other specialties to ascribe facial pain and headaches to sinus disease. Chronic pharyngitis and laryngitis with the patient complaining of a productive cough are often encountered. hypertension. cervical spine disorders. Chronic irritation of the nasal airway and repeated rubbing may lead to a vestibulitis and epistaxis. In this group of patients nasendoscopic examination with a high-definition coronal section CT scan may confirm that the symptoms are indeed sinus related. a steroid nasal spray. 2. Functional endoscopic sinus surgery is now the preferred alternative to the classical open surgical approaches to chronic sinusitis. The patient may also suffer with anosmia. The cardinal symptoms are nasal congestion. Clinical examination will usually show nasal inflammation or perhaps another obvious intranasal predisposing factor.288 OTOLARYNGOLOGY this time may be irreversible. neoplasm. neuralgias. and when the original cause of infection has been treated the lining will not revert to normal. for example rhinitis or nasal polyps. or even cacosmia (unpleasant smell). Mucosal thickening occurs in 30% of individuals and its detection is often meaningless. Surgery (a) Functional endonasal sinus surgery. Any obvious predisposing factor.

The earlier the treatment is started. The natural ostium of the maxillary sinus in the middle meatus can be cleared. 2. may also be useful. Usually associated with nasal polyps and asthma. Bipolaris and Curvularia. • Chronic ethmoid sinusitis: intranasal ethmoidectomy. • Chronic sphenoiditis: via an intranasal ethmoidectomy. (b) Open sinus surgery procedures. but details of each procedure and its complications should be sought from an operative textbook. so the choice of operation should be tailored to the requirements of the individual patient. This should be suspected in a healthy patient presenting with chronic sinusitis resistant to conventional therapy. Amphotericin B is the drug of choice. leukaemia and lymphoma). Aspergillus fumigatus is the most common organism isolated. 4. They are listed below. transantral to the posterior ethmoids then to the sphenoid sinus. However. 3.SINUSITIS 289 can be undertaken. Fungal sinusitis This is now being recognized more frequently. • Chronic maxillary sinusitis: Caldwell-Luc procedure. appropriate treatment needs to be rapidly instituted. Fungal sinusitis can be divided into the following entities: 1. the better the prognosis. the more radical open procedures are still used and asked about in the examinations. external ethmoidectomy (Patterson’s operation). Acute invasive (fulminant) sinusitis. The mainstay of therapy is polypectomy and aeration of the sinuses. Allergic fungal sinusitis. These are masses of fungal debris that usually occur in the maxillary or ethmoid sinuses. . This is a slow progressive disease characterized by granulomatous infection. Associated fungi include Aspergillus. Mucor and Rhizopus are the associated organisms. There is usually no requirement for antifungal or any other systemic therapy. • Chronic frontal sinusitis: external frontoethmoidectomy (Howarth’s operation). chemotherapy patients. Surgical debridement with removal of all debris from the sinuses is required. which can extend to a total maxillectomy and orbital exenteration. Aspergillus fumigatus is the most common organism isolated. opened and enlarged. osteoplastic flap procedure (MacBeth’s operation). Systemic steroids and antifungal therapy (itraconazole). Patients are typically immunocompetent and non-atopic. Immediate treatment consists of intravenous antifungal therapy (amphotericin B) and radical surgical debridement. because of advances in diagnostic techniques (nasal endoscopy and CT scans) and increasing numbers of immunocompromised individuals. Aspergillus. A wide range of procedures are available. The disease still carries a mortality rate of 50–80%. Treatment is by endoscopic removal of debris and ventilation of the sinus. Chronic indolent sinusitis. Typically occurs in atopic immunocompetent young adults. via an external frontoethmoidectomy. transantral (Horgan’s operation). Mycetoma. Because of the potential for orbital and intracranial complications. A rare entity that occurs in immunocompromised individuals (diabetic ketoacidosis. as can any disease of the frontonasal duct. Each procedure has its own limitations and specific complications. If irreversible changes have occurred to the sinus mucosa then some surgeons would consider it necessary to remove it. AIDS.

p. 131. p. Headaches and sinus disease: the endoscopic approach. Sinusitis— complications. Functional endoscopic sinus surgery. . Rhinology and Laryngology. Annals of Otology. Intrinsic rhinitis.290 OTOLARYNGOLOGY Further reading Durand M. 97 (Suppl. 5:8–12. 291. Current Opinion in Otolaryngology and Head and Neck Surgery. p. 134). 1997. 1988. 108. 11. The antibiotic treatment of sinusitis. p. Related topics of interest Allergic rhinitis. Stammberger H and Wolf G.

The ethmoids are separated from the orbit by the thin lamina papyracea. Elevation of the orbital periosteum usually reveals the pus under pressure. Colour blindness is an early sign. Orbital complications These can occur at any age. A subperiosteal abscess results from direct spread from the ethmoids and collects between the lamina papyracea and the orbital periosteum. The biggest anxiety is the risk of blindness as a result of tension and septic necrosis of the optic nerve. A CT scan will confirm the collection and extent of the disease. They can be divided into: • • • • • Orbital complications (orbital cellulitis and orbital abscess). visual fields. Urgent surgical drainage is indicated. If the other eye is stimulated but there is no contralateral reflex. Absence of the ipsilateral and contralateral light reflex will occur with visual impairment. then the third cranial nerve (occulomotor) will have been affected. laryngitis. red-green colour vision. An external ethmoidectomy is performed and a drain inserted. Cellulitis requires treatment with intravenous antibiotics and nasal decongestants to resolve the infection and limit further spread.SINUSITIS—COMPLICATIONS In most cases sinusitis is uncomplicated and spread of infection beyond the walls of the sinus is uncommon. Complications may follow an acute infection. With an orbital collection the eye will become proptosed and its movements progressively restricted to a complete ophthalmoplegia. The swelling may displace the orbit lateral and down. but are most frequent during an acute exacerbation of chronic sinusitis. Aching around the orbit is followed by oedema of the eyelids and later the conjunctiva. otitis media). Early liason with an ophthalmologist is recommended. but are more common in children. pupillary reflexes. An incision is made in the superomedial aspect of the orbit. and the optic disc should be examined. . Visual acuity. Peri-orbital cellulitis and orbital abscess usually result from direct spread of pus from the ethmoid sinuses. Intracranial complications (meningitis. cavernous sinus thrombosis). Osteomyelitis (maxilla or frontal bone). Mucocele. It can also spread from thrombophlebitis of mucosal vessels in any of the sinuses. intracranial abscess. Locoregional complications (pharyngitis. Synchronous infection of the maxillary sinus may require treatment with intravenous antibiotics and surgical drainage (usually an endoscopically fashioned middle meatal antrostomy and sinus washout). The orbital septum forms a natural barrier which may localize the infection anteriorly as a preseptal cellulitis or posteriorly as orbital cellulitis.

but it is essential to exclude raised intracranial pressure before this is done by looking for papilloedema. A CT scan with enhancement or MRI scan may assist in diagnosis. especially the orbit. An endoscopic approach is an alternative in experienced hands. To approach the frontal sinus. It occurs most commonly in the frontal sinus. The cyst gradually expands and exerts pressure on the sinus walls causing erosion. A subperiosteal abscess of the forehead may form (Pott’s puffy tumour). subdural or cerebral) and cavernous sinus thrombosis may complicate sinus infections. IV. Meningitis is the commonest complication. The common organism is Staphylococcus aureus. particularly in sinusitis patients who become drowsy or show some neurological deficit. reduced conscious level and cerebral irritation. but encephalitis. . The clinical features of meningitis are well known. An intracranial abscess may be more difficult to diagnose. The main complaints are headache and swelling.292 OTOLARYNGOLOGY Osteomyelitis This only occurs in diploic bone and thus only in the maxilla of children and the frontal sinus of adolescents and adults. the two options in common use are external fronto-ethmoidectomy (Howarth’s operation) and the osteoplastic flap procedure (Macbeth’s operation). This leads to displacement of adjacent structures. Mucocele A mucocele may develop when the outlet from a sinus becomes permanently blocked. Up to 25% of patients may die and nearly a third of surviving patients will suffer with epilepsy. An extradural or subdural abscess will require drainage by a neurosurgeon. These features can be dramatic if infection supervenes (pyocele). ophthalmic and maxillary branches of V and VI). Radiographs will show enlargement of the sinus with thinning of the bone. Prompt treatment with high doses of intravenous antibiotics. It presents as a painful swelling of the cheek and lower eyelid. A lumbar puncture may identify the causative organism. Treatment comprises intravenous antibiotics and debridement when necessary. Osteomyelitis of the maxilla is rare and usually only seen in third world countries. together with drainage of the offending sinuses by an ENT surgeon. and appropriate debridement is required. Infection may involve the brain and meninges from either direct spread or retrograde thrombophlebitis. The eyes will proptose and an ophthalmoplegia of the cranial nerves which travel in the cavernous sinus will occur (III. High resolution CT scan and MRI will illustrate the extent of the problem. CT scans will further delineate the extent of the disease if needed. surgical drainage of the frontal sinus. This is a life-threatening condition with a high risk of intracranial complications. ethmoidal and sphenoid sinuses are closely related to and separated by a thin wall of bone from the anterior cranial fossa. The important point is that the ENT surgeon should always maintain a high index of suspicion for all intracranial complications. There is a build-up of dull local pain with oedema of the forehead and the upper eyelids. Intracranial complications should all be treated with high-dose intravenous antibiotics. Diplopia and proptosis may result if the mucocele expands into the orbit. intracranial abscess (extradural. Cavernous sinus thrombosis will cause a high fever. but the ethmoid. Treatment is surgical evacuation and drainage of the sinus. There is an accumulation of sterile mucus which becomes increasingly viscous. Osteomyelitis of the frontal bone is more extensive and dangerous. maxillary and sphenoid sinuses can all be afflicted. The mortality and morbidity after intracranial complications is considerable. Intracranial complications The cavities of the frontal.

4. Swift AC. Vol. 1998:868–883. Scott-Brown’s Otolaryngology. Related topics of interest Sinusitis. Further downward spread may lead to irritation of the vocal cords causing a laryngitis. p. The complications of sinusitis. Further reading Lund VJ. Sinusitis is also implicated as a cause and complication of tonsillitis and otitis media. 285. Nose and Throat. Invasion of the subepithelial lymphoid tissue will produce a granular pharyngitis with visible nodules as the lymphatic tissue hypertrophies. p. The complications of sinusitis. In: Diseases of the Head and Neck. London: Arnold. Functional endoscopic sinus surgery. . 6th edn. Jones AS (ed). Bull TR (eds).SINUSITIS—COMPLICATIONS 293 Locoregional complications Regional complications occur as a result of infection and inflammation spreading through the rest of the upper aerodigestive tract mucosa. 1–11. In: Mackay IS. 1997. Mucopus from sinusitis is carried back through the nasal airway into the pharynx and may cause a pharyngitis. 108. London: Butterworths.

sweet and S on the anterior tongue and sour on the lateral border. with their primary afferents synapsing in the tractus solitarius in the medulla. Gustation. thermal or chemical stimuli. These fibres are stimulated by (unpleasant) mechanical. Several different cranial nerves are involved. 3.SMELL AND TASTE DISORDERS There are three chemosensory portions to smell and taste: 1. Bitter tastes are better perceived on the posterior tongue. It is known. 2. Degradative enzyme systems appear to exist for stimulant breakdown after neural interaction. It is likely that all these factors have a bearing on smell recognition. 3. resulting in the production of an intracellular secondary messenger (usually cyclic AMP). Neural stimulation occurs after dissolving of the tastant in a similar fashion to olfaction although the neural pathways are more complex. They may then dissolve in and diffuse through the overlying mucus or they may combine with specific odorant-binding proteins and be transported through the overlying mucus layer. with subsequent cell depolarization and a neural action potential. . Olfaction. The free molecules or odorant/protein complexes then attach to receptor proteins. however. Gustation (taste) is served by the taste buds. Common chemical sensation. Common chemical sensation (irritation and textural quality) is served by free nerve endings from branches of the trigeminal nerve in the oral cavity and nose with a contribution from the glossopharyngeal and vagus nerves in the oropharynx. Information is ultimately passed to the cortex via the thalamus. although there are regional differences in their concentration and distribution. Quite how this sensory information codes for smell is unknown. hypothalamus and cortex. neither are they equally distributed in the nasal cavity. 2. Olfaction (smell) is provided by a small area of olfactory epithelium in the vault of the nasal cavity. that different odorants have different rates and degrees of solubility in the overlying mucus. The olfactory neurones pass through the cribriform plate and sensory information passes to the olfactory bulb and then on to the thalamus. Physiology 1. Not all olfactory receptors respond equally or at all to different odorants. Recent research has postulated that there are certain ‘groups’ of smells that might be recognized by a relatively common mechanism. before sensation passes on to the thalamus and cortex. which are modified epithelial cells found throughout the oral cavity. Odorant molecules (those molecule with the ability to bind and stimulate olfactory receptors) are carried into the nasal cavity with (inspiratory and expiratory) airflow.

Management Sinonasal disease should be managed as appropriate to the condition. previous nasal surgery. Most losses of taste that patients complain of are in fact loss of olfaction. in the sense of smell or taste. (Neural). Reassurance regarding the absence of serious pathology should be stressed to the post-URTI and head injury groups. Further general investigations will be dictated by the clinical features. lemon or coffee.SMELL AND TASTE DISORDERS 295 Pathology It is uncommon for common chemical sensation or taste to be lost. Head injury (20%). including systemic disease. For example. Olfactory disturbances tend to be more common with increasing age and fall into three main groups: impaired transport. In most cases this is due to simple mechanical obstruction (polyps. Sinonasal disease (20–30%). sensory and neural. Management of any systemic causes is as for that condition and drug-induced problems may require a change of medication. although in some cases the local inflammatory response may alter the overlying mucus or the function of the receptor cells. It has the best prognosis in terms of response to treatment. mucosal swelling in rhinitis. peppermint. Clinical features The patient may complain of loss (anosmia). Serious head injury can result in shearing of the olfactory filaments as they pass through the cribriform plate or direct contusion of the olfactory bulb or cortex. e. Probably due to damage of the peripheral olfactory receptors following infection with a neuropathic virus. The sense of smell can be crudely tested using a variety of recognizable odours. cloves. metabolic and connective tissue disorders. 3. Commercial ‘scratch and sniff’ kits are available using a forced choice technique which greatly increase their sensitivity. toxin exposure. 5. diminution (hyposmia) or alteration. Investigations A thorough history must be taken and any temporal relation to an upper respiratory infection or head injury noted. It is important that the test scents are not too pungent or irritant (e. Some objective measure of olfaction is helpful. Little is known about the idiopathic group and certainly no treatments . there is much redundancy in the neural supply and the sensory distribution is relatively wide. It is more likely that olfaction may be lost or impaired.g. etc. radiotherapy and old age. usually unpleasant (parosmia). Radiological imaging (including CT scans) of the sinuses may be required. bleach) as they may then be recognized by common chemical sensation. as do those following head injury. (Transport). (Sensory).) preventing odorants from reaching the olfactory epithelium in the narrow nasal vault. 4. A small proportion in both groups (10–20%) will improve with the passage of time. Hyposmia is a more common symptom following URTI. Following upper respiratory tract infection (15–20%). neurological conditions.g. Idiopathic (20%). A multitude of other causes exist. they can be useful for deciding if a patient is suffering from anosmia or is malingering. A full nasal examination including endoscopy will be required to establish any sinonasal disease. In this last case the patient is often confusing taste with flavour as taste is rarely lost. The majority of patients (60–75%) with sinonasal disease describe anosmia rather than hyposmia. 2. Others (15–20%). drug therapy. The main causes of disorders of smell and taste are as follows: 1.

75:1321–1348. Smell and Taste in Health and Disease. p. Intrinsic rhinitis. 115. Related topics of interest Allergic rhinitis. p. Medical Clinics of North America. Disorders in taste and smell. Some authorities claim that a trial of zinc supplements should be administered. Leopold DA. 1991. 11. Bartoshuk LM and Snow JB (eds). New York: Raven Press. Halitosis. Getchell TV. but some surgeons will see if the patient has any response after a trial of using a steroid nasal spray. Doty RL. . Follow-up and aftercare This should be as appropriate for the underlying cause. p. Further reading Mott AE.296 OTOLARYNGOLOGY are available. 1991. 174. Nasal polyps. p. 131.

which is an attempt to overcome the obstruction and if frequent results in poor sleep quality. Any cause of airway narrowing from nares to glottis can contribute to increased airway resistance. ceases for a period of time. hypoxia. increased negative intrathoracic pressure and increased cardiovascular strain. Pathophysiology The noise of snoring is produced by vibration of the soft palate and pharyngeal walls caused by turbulent airflow and the Bernouli effect from a partial obstruction. arousal. .SNORING AND OBSTRUCTIVE SLEEP APNOEA M. 2. Apnoea:a period of no airflow at the nose or mouth for at least 10s. Sleep apnoea can be obstructive. Sleep apnoea syndrome can be diagnosed if there are more than 30 apnoeic episodes in 7 h of sleep or if the apnoea index is more than 5. 3. In central apnoea. In obstructive sleep apnoea (OSA) there is complete upper airway obstruction yet the patient continues to make respiratory efforts to overcome this. It is a symptom of serious neurological disease and is not considered further here. the Venturi effect and the decreased muscle tone associated with sleep can all predispose to upper airway collapse. Central apnoea is due to a defect of autonomic control of respiration in the medulla or peripheral chemoreceptors resulting in a failure of respiratory drive. respiratory effort. Hypopnoea: 50% or greater reduction in normal tidal volume. which may cause cardiac dysrhythmias and if severe and prolonged may lead to pulmonary and systemic hypertension and cor pulmonale. Sleep apnoea is classified as mild (AI=5–20). moderate AI=20–40) or severe (AI > 40). Apnoea index (AI): the number of periods of apnoea per hour.Pringle Definitions • • • • Snoring: a noise generated as a result of partial upper airway obstruction during sleep. central or mixed. The obstruction occurs when the negative intraluminal pharyngeal pressure exceeds the ability of the dilators to hold the pharynx open. Neuromuscular incoordination interfering with the reflex activity of the pharyngeal dilators associated with inspiration. increased compliance of pharyngeal tissues. and consequently airflow. This obstruction has three effects: 1. As a consequence patients with severe OSA are at risk from increased mortality due to cardiovascular disease.

Treatment Snoring and OSA are often multifactorial conditions with a variety of primary causative factors. oxygen saturation. The manoeuvre is then repeated with the endoscope positioned just above the soft palate (velopharyngeal level). Palatal surgery is far less effective in patients with a body mass index of > 30. body position monitor and microphone recording of the snoring. Site of obstruction. ECG. electromyogram (EMG) (to detect periodic limb movements). Probably the most widely used test is the Muller manoeuvre. hence there will never be one single universal cure for snoring. sleep nasendoscopy. Polysomnography is the gold standard and involves recording an electroencephalogram (EEG). intellectual deterioration. In children it most commonly occurs around the age of 5 years when lymphoid hyperplasia is at its greatest. To identify sleep apnoea. endocrine disorders. • General Patients with simple snoring and mild OSA can be reassured that there is no evidence of long term health risk. 4.298 OTOLARYNGOLOGY Clinical features Snoring and OSA in adults is more common with increasing age. while taking the history it is preferable to have the bed partner present. personality change. in men. 3. Snoring occurs in 10% of men under 30 years of age and 60% of men over 60 years of age. The latter two are research tools. For some patients this reassurance will be enough others will request further treatment. To differentiate between palatal and tongue base or multi-segmental obstruction. These consider full blood count (FBC). An overnight sleep study. in the obese and in those with a high alcohol intake. The patient inhales vigorously while the nares and mouth are occluded and the degree of hypopharyngeal collapse noted. This is expensive in terms of time and equipment but is an ideal research tool. General investigations. One technique involves overnight video recording. This involves positioning per nasally a flexible fibreoptic endoscope to the level of the tongue base with the patient in the sitting position and with the mouth closed. obese=30–40. OSA often leads to excessive daytime somnolence. a variety of tests have been developed including lateral cephalometry. Body mass index (BMI). while OSA can be found in approximately 6% of men. Effective screening sleep studies may be performed excluding EEG and EMG. It is important to establish whether the patient has simple snoring or OSA. This measurement helps define degree of obesity. A thorough history and examination is needed. Investigations 1. It is calculated by dividing the weight in kilograms by the height in metres squared (Kg/m2). Overnight pulse oximetry will detect all those with severe OSA but may miss some with moderate OSA. very obese = > 40. 2. impotence and an increased risk of a road traffic accident. thyroid function tests (TFT). morning headaches. electrocardiogram (ECG). In this way the level of obstruction can be identified in up to 85% or cases. . Normal BMI=19–25. cine CT and somnofluroscopy. abdominal and chest movements. airflow. It does not detect arousal’s (which are triggered by high negative intrathoracic pressure rather than hypoxia) and may miss ‘high upper airways resistance syndrome’ (HUARS). Accurate assessment is essential to guide treatment. overweight=26–30. chest radiograph. to exclude any exacerbating factors (drugs. Snoring can be immensely socially disruptive and may lead to marital difficulties. This is probably because these patients are more likely to have OSA with multisegmental or tongue base level collapse. manometry. anatomical) and to identify the site and level of obstruction.

Somnoplasty. when all other forms of treatment have failed. though long term rates are around 50%. i. • Maxillofacial. This surgery can be very painful and complications include nasopharyngeal reflux and dry mouth. turbinate hypertrophy or nasal polyps may all help snoring by overcoming nasal obstruction. It can be extremely effective but compliance is often a problem. • Oropharyngeal obstruction causing simple snoring and OSA. • Tracheostomy. Laser palatoplasty involves excision of the uvula and scarring of the soft palate with the laser in a variety of ways to induce palatal stiffness. OSA is in most cases adequately dealt with by adenotonsillectomy as this is the usual site of obstruction. It is recommended for certain individuals with simple snoring. • Nasal obstruction. Uvulopalatopharyngoplasty (UPPP) involves tonsillectomy and excision of the uvula. In severe OSA. If nasal CPAP or pharyngeal surgery are contemplated any nasal obstruction should be corrected first. This may be related to later weight gain. though this can not be guaranteed. ii. i. Air under pressure is delivered via a tight fitting nasal mask. • In moderate to severe OSA due to tongue base and multisegmental airway collapse surgery is not particularly effective and anaesthetic risk is significant. Medical treatment of rhinitis. In appropriately selected patients all these procedures have a 70–80% success rate. the use of the “Nozovent” nasal splint or Breathe Right nasal strips to open the nasal valve or surgical correction of a septal deviation. Adenotonsillectomy. LAUP (laser assisted uvulopalatoplasty) is a technique in which the uvula is vapourised by the laser and troughs created through the soft palate to each side of the uvula base to form a neouvula. Hyoid suspension techniques to advance the hyoid and hence move the tongue base forward have been tried with some success. In patients with morbid obesity and life threatening obstructive sleep apnoea bi-maxillary and bimandibular advancement osteotomies have been performed together with significant success rates reported. This in turn draws the tongue base forward enlarging the pharyngeal airway. With a history of OSA sedative pre-med should be avoided. This results in an area of scarring and hence stiffening of the soft palate. Long term effects on the temporomandibular joints are not known. it can significantly improve a patients quality of life. A new technique in which low temperature radio-frequency energy is delivered via a needle placed into the soft palate.SNORING AND OBSTRUCTIVE SLEEP 299 Weight loss is very important and advice with regard to alcohol and sedative medication are often helpful especially in patients with OSA. LAUP is sometimes performed under a local anaesthetic. Nasal Continuous Positive Airways Pressue (nasal CPAP) is the gold standard treatment. In children. Despite the procedure. Early results are encouraging but there are no long term studies. The air acts as a pneumatic splint holding the upper airway open and preventing snoring and obstructive episodes. iv. Mandibular Positioning Devices. In retrognathia mandibular osteotomies may be required. ii. . This appliance is worn in the mouth overnight It is like an upper and lower gum shield attached in such a way as to hold the lower jaw forward. a tracheostomy can be lifesaving. iii.

Scott Browns Otolaryngology.B. Tracheostomy. p. . 1–22. 333. Pringle M. Tonsillectomy.B. p. p. Related topics of interest Adenoids. 8..300 OTOLARYNGOLOGY Further reading Croft C. pp. 336. 1997. Snoring and sleep apnoea. 6th edn.

Medical Research Council. Boothroyd and Manchester junior word lists. Speech audiometry provides a measure of this ability and any corresponding deficit. It is useful in a variety of contexts including: • • • • Assessment and diagnosis of peripheral and central hearing disorders. ah. Standardized. The main function of the human ear is therefore the perception of speech. in general. speech audiometry implies the formal qualitative assessment of a subject’s perception of speech. prepared speech material presented by cassette and controlled by the audiometer is much more preferable. Materials 1. Testing is performed in a soundproof room using a cassette player or microphone with the volume controlled from the audiometer which presents speech material to the subject via loudspeakers or headphones. as opposed to the free-field situation with loudspeakers. It measures the actual disability produced by the hearing impairment. most of the handicap of hearing loss is due to loss of the ability to perceive the spoken word. Fry. Medicolegal assessment. Masking sounds in speech . Instruments. Speech material is chosen to provide a representative balance of phonemes and can be presented as words.g.g. Indeed. the ear is specifically tuned to the speech frequencies (500–4000 Hz). Institute of Hearing Research. Speech material. However. The recorded word lists are presented to the patient monaurally over headphones at various sound intensities. In the human. sentences or synthetic sentences which have no meaning. and Bench. etc. Speech material presented by the tester using a microphone is prone to variation in both intensity and accent. ay. Phonemes are the building blocks of speech and represent the smallest unit of recognizable speech sound (e. 2. Koval and Bamford (BKB) sentences (University of Manchester). allows each ear to be tested individually and allows the non-test ear to be masked.). Voice tests can be considered as a very basic form of speech audiometry. Procedure The subject is seated in a soundproof room and instructed in the test procedure. The use of headphones.There are 49 phonemes in the English language. masking of the non-test ear is required on all occasions. Prediction of the usefulness of a hearing aid. Evaluation of the benefit which might be obtained by an operation (pre.and postoperative assessment). A great number of lists of appropriate speech material have been developed by various agencies e. aw. As speech audiometry is a suprathreshold test.SPEECH AUDIOMETRY In many animals the sense of hearing is adapted for a specific purpose.

+20. no matter how loud the volume is turned up. . Scoring (a) The optimum discrimination score (ODS) is the subject’s maximum score. It is a measure of optimal performance and should be 100% when normal. Two tests exist: (a) Delayed speech feedback (DSF). cocktail party and babble noise. Pink noise (equal energy for each octave over the hearing range) is often used when these are unavailable.302 OTOLARYNGOLOGY audiometry are chosen to try and recreate an appropriate noise background such as speech. (c) The half-peak level (HPL) refers to the sound level (dB) at which the discrimination percentage is half the ODS. The recorded data can then be used to formulate certain scores and the shape of the graph used to give information regarding the type of deafness. but they must be played louder than for a normal subject. This type of curve is typical of a retrocochlear lesion.e. (d) The half-peak level elevation (HPLE) refers to the difference between the pathological and normal HPL. (b) The speech reception threshold (SRT) is the sound intensity (dB) at which the subject can correctly repeat 50% of the presented words. Speech audiometry can be used in the investigation of non-organic or feigned hearing loss. The graphical display is compared with the calibration graph for that particular machine. Specific uses 1. and consequently the ODS is often less than 100%. The curve is parallel to the normal but is shifted to the right (i. although more may be required. near-vertical portion in the middle. which will have been obtained by testing otologically normal individuals on that machine. In severe cases ‘roll over’ may occur: beyond a certain point any further increase in sound intensity causes a reduction in the discrimination score. Subsequent presentations are usually made at +10. This is considered to be the most valuable diagnostic score. -10 and -20 dB from this level. stammering and a raised voice are almost inevitable. In patients with a conductive hearing loss all the words will be understood. The result is a sigmoid-shaped curve with a steep. The patient is asked to repeat the words as accurately as possible and the percentage of words or phonemes which are correctly repeated at each sound intensity (dB) is calculated and plotted on a graph. If there is normal hearing in the test ear. The speech is relayed to the test ear with a delay of 1–200 ms. The ODS is still 100% as discrimination is preserved. Non-organic hearing loss. The gradient of the middle portion of the curve is often less and a plateau may be reached in which further increases in sound intensity do not improve discrimination. This is the dB level at which the patient achieves half the ODS in comparison with the level at which normal individuals achieve 50%. The subject is asked to read text aloud. greater HPL) in proportion to the degree of hearing loss. In patients with a sensorineural hearing loss there is usually a loss of ability to discriminate speech. The first presentation is usually at 20–30 dB greater than the pure-tone average for the frequencies 500. using the same tapes and test environment. 1000 and 2000 Hz. Shape of the graph If the hearing is normal all the words will be understood if they are played loudly enough.

This can be done using a variety of techniques. 45. If the hearing is normal. Pure tone audiogram. For further details on this. p. 2. p. stuttering is likely when the competing material is 40 dB louder than the test material. interrupted and filtered speech. Further reading Ballantyne D. Central auditory function. 194. 1990. 1991. Pensak ML. Related topics of interest Acoustic neuroma. p. London: Butterworth-Heinemann. the reader is referred to Keith and Pensak (1991). 254. Keith RW. accelerated. . including speech messages in competing noise. p. Non-organic hearing loss.SPEECH AUDIOMETRY 303 (b) Competition tests. Handbook of Audiological Techniques. Speech audiometry can also be used as a test of central auditory function. competing messages and overlapping messages in each ear. Central function. 24(2): 371–379. The patient is asked to repeat speech material delivered to the good ear while competing speech material is introduced to the test ear. Clinical assessment of hearing. 1. Otolaryngologic Clinics of North America.

volume. It can be a long-term option when the pharyngo-oesophageal (PE) segment is not viable. developing compensatory articulation strategies with patients who have had oral surgery. 2.Young The speech therapist is a member of the multidisciplinary rehabilitation team. The main aims of rehabilitation are to ensure that patients have optimal communication skills. • oesophageal voice.g. 3. articulation. stomach pull-up. assessment and therapy for patients who have dysphagia following head and neck surgery. Electrolarynx The electrolarynx is useful as a temporary measure before oesophageal voice is functionally adequate or before placement of a voice prosthesis. Factors such as speech rate. The role of the speech therapist working with patients under-going head and neck surgery is essentially threefold: 1. There are three options for alternative voice: • electrolarynx. e. motivation and communication needs can have a significant bearing on the prognosis for rehabilitation of communication. Training is needed to develop accurate placement of the device. education and support pre-operatively. or when it is the patient’s preference. improve articulatory precision and to establish appropriate phrasing.SPEECH THERAPY IN HEAD AND NECK SURGERY P. tension levels. the rehabilitation of voice. Hard fibrotic post radiotherapy/ surgery neck tissue will prevent transmission of sound into the oral cavity. following laryngectomy. posture. . Efficient use of the electrolarynx is mainly dependent on neck status. reduce speech rate. oro-mandibular function and are able to swallow. Voice rehabilitation following laryngectomy Ideally laryngectomy patients (and their relatives) should be seen by the speech therapist for assessment. in cases of radical surgery where prosthesis placement is contraindicated. • surgical voice restoration (SVR) with a voice prosthesis. An oral examination and communication profile are carried out. hearing.

such that when the stoma is occluded pulmonary air is transmitted through the catheter to below the PE segment. rate. consistency and volume which can be achieved with a voice prosthesis using pulmonary air. articulation. This test can also be carried out before commencing oesophageal voice training as it provides information about the tonicity of the PE segment. and modifying the speech rate and phrasing to maximise intelligibility. This means that much of the frustration. voice quality. who also rates tension levels. i. Surgical voice restoration Oesophageal voice lacks the duration. There must be adequate apposition of the oesophageal mucosa to form a functional PE segment.g. Evaluation of the voice is carried out at regular intervals. pitch (where instrumentation is available). fluency. which is glued to the stoma. breath/voice co-ordination. i. After valve placement speech therapy involves: training in maintaining the valve. The patient has to learn to dissociate respiration from phonation. Blom-Singer and Bivona. The acquisition of a functional oesophageal voice can take months of intensive speech therapy. The tonicity of the segment determines the quality of the voice achieved and the effort necessary to produce it. including objective measurement of: • • • • • duration. In SVR.e.g. achieving accurate occlusion of the stoma. e. and certain adept patients can be trained to change their own valves. maximum phonation time: how long the patient can sustain a vowel on one breath.e. The amount of air pressure needed to produce a voice and the fluency and durability of the voice achieved are noted. e. There can be difficulties at any stage in this process. expired pulmonary air passes through the one-way silicone valve in the tracheo-oesophageal wall. availability of the voice. to what extent are they able to use their voice with confidence in all situations. When secondary placement is planned. Provox and Blom-Singer Groningen button. etc. Many centres now favour primary placement of the prosthesis during laryngectomy so that patients can leave the hospital with a voice.SPEECH THERAPY IN HEAD AND NECK SURGERY 305 Oesophageal voice Both oesophageal voice and SVR require a viable PE segment or neoglottis. ease of initiation. Provox II.g. the speech therapist or ENT surgeon carries out an air insufflation test (Taub and Bugner. Voice prostheses are of two main types: the non indwelling type. depression and strain on relationships caused by a lengthy period of postoperative aphonia can now be avoided. Indwelling valves. fluency. The oesophageal speaker has to gain voluntary control of the PE segment in order to take air into the upper oesophagus. and much more commonly the in-dwelling type. 1973). The patient is asked to speak. A catheter is inserted via the nose to the level of the stoma and is connected to a housing. The air is then released. when the stoma is occluded. i. Ultimately the success of voice rehabilitation is a measure of patients’ satisfaction with their communication. Intelligibility and communication skills can be rated subjectively by naive listeners or by the speech therapist. dynamic range (volume).e. producing sound as it passes through the PE segment. . It is then amplified by the resonating spaces and modified by the articulators in the normal way. the number of syllables produced per breath on air charge. e. setting the PE segment into vibration. The segment is composed of the inferior constrictor including cricopharyngeus and the upper oesophagus. can now be changed by a speech therapist/specialist nurse via the stoma.

Post-operatively. These compensations are then practised for integration into spontaneous speech. speed and accuracy of movement of lips. When healing is complete a bedside assessment of the swallow is carried out to identify the risk of aspiration. e.g. e. postures and manoeuvres on the efficiency and safety of the swallow. symmetry and clearance of the pharynx at rest and post swallow. Access to videofluoroscopy or modified barium swallow is essential with this patient group. Members of the club also carry out pre and post-operative visits to new patients. • sample swallows observing oral manipulation. swallow initiation/delay. strength. Most speech therapy departments organise a club for their head and neck patients aimed at providing information. support and social activities on a long-term basis. • assessment of sensation in tongue. It permits full evaluation of oropharyngeal anatomy and impaired swallow physiology. When alternative feeding methods are necessary to maintain nutrition. the speech therapist continues to rehabilitate the swallow with the gradual re-introduction of oral intake when safe. when.306 OTOLARYNGOLOGY There is no doubt that the best possible voice results are obtained with a voice prosthesis. once healing is complete. tongue and palate. . Follow-up and aftercare Follow-up as an out-patient or on a domiciliary basis should be available for as long as is necessary for this patient group.g/ phonemes in a glossectomy patient. clinical signs of penetration (substance entry into the airway above the vocal cords) and aspiration (before. The available alternatives are not mutually exclusive. laryngeal elevation. Surgical dysphagia The speech therapist should see any patient pre-operatively when post-operative dysphagia is anticipated. Compensatory articulatory strategies following oral surgery All patients should be seen pre-operatively so that the therapist can obtain a sample (preferably taped) of the patient’s speech.g. the use of a uvula sound as a substitute for / k. why and how much. The speech therapist then works on improving excursion and control of available articulators and systematic exploration of potential compensatory articulations which will improve the patient’s ability to make phonemic contrasts and hence improve intelligibility. It confirms whether aspiration is occurring. but individual ENT departments have to decide which is to be their method of choice and ensure that the other alternatives are available to patients if the first option is either contraindicated or unsuccessful. Fees (fibreoptic endoscopic evaluation of swallowing) is useful to assess the anatomy. This includes: • evaluation of the range. lips and palate. oral transit time. patients are assessed using phonetically balanced word lists to establish an objective measure of their intelligibility across all the phonemes of English. during and after the swallow). The speech therapist can observe the impact of compensation techniques and therapeutic manoeuvres and make recommendations accordingly. but these are not without complications and the patient remains dependent on the hospital for maintenance of the voice. gastrostomy. • the effect of modified textures.

to assist patients to compensate and adjust to their new set of circumstances. p. 2:216–219. Laryngeal carcinoma. Dysphagia. 1984. Oral cavity carcinoma. Schartz K. p. p. Related topics of interest Hypopharyngeal carcinoma. American Journal of Surgery. Bugner LH. 138. 1993. 1983. p. p. Laryngectomy. Laryngectomy. Olsen N. 197. 203. Taub S. 124. Air bypass voice prosthesis for vocal rehabilitation of laryngectomees. Logeman J. Dysphagia—Diagnosis and Management. Manual for the Videofluoroscopic Study of Swallowing.SPEECH THERAPY IN HEAD AND NECK SURGERY 307 Eating and talking are not only essential but pleasurable activities. The Evaluation and Treatment of Swallowing Disorders. and it is important not to underestimate the trauma suffered by patients who have problems with either of these functions. . 143. The aim of speech therapy is to achieve maximum rehabilitation and. San Diego: College Hill Press. London: Butterworths. 125:748–756. Austin TX: Pro-Ed. Oropharyngeal carcinoma. A new procedure. 1973. Further reading Groher ME. Fibreoptic endoscopic examination of swallowing safety. Langmore SE. where preoperative functional levels are not achievable. In: Edels Y (ed). Logeman J. 1988.

Untreated. typical symptoms (e. The latter group of voice disorders are characterised by habitual misuse of the voluntary muscles of the larynx and pharynx and have been classified by Morrison and Rammage (1994) as muscle tension dysphonias. nodules. Conditions which do not respond well to voice therapy . Reinke’s oedema (mild). Previously. visible on laryngoscopy which can be attributed to a particular pattern of underlying muscle misuse. Referral to speech and language therapy All patients with a voice disorder. In the light of the above it is important that referral should include not only a description of the structure of the larynx and any organic changes. Puberphonia. these problems can progress to organic changes (e. the patients occupation is important to note as most speech therapy departments will prioritise professional voice users for therapy. oedema. vocal nodules) and other presentations where no structural changes could be observed would be classified as ‘functional dysphonia’. but also the glottic shape observed on phonation.g.g.g. Conditions that respond well to voice therapy • • • • • • • • Muscle tension dysphonias (e. Globus sensation. If these patients are treated early.Young In recent years. Chronic laryngitis. False cord phonation (dysphonia plicae ventricularis). Together with any relevant ENT findings and previous medical history. posterior glottic chink.g. significant progress has been made towards the understanding of the function and dysfunction of the human voice and applying this new knowledge and technology in the clinical evaluation and treatment of voice pathology. chronic laryngitis. Psychogenic aphonia. vocal cord bowing). mild dysphonia and discomfort with prolonged talking) can be treated successfully. with the exception of transexuals must be referred by an ENT surgeon. ENT consultants would diagnose organic problems descriptively (e. They describe six typical glottic and supraglottic postures. pitch breaks. Early/soft vocal nodules. etc).SPEECH THERAPY IN NON-MALIGNANT VOICE DISORDERS P.

the patient’s general health. and any predisposing factors. Patients can view their larynx on a TV monitor. resonance. Hard. . and using nasendoscopy. glottal attack. or rigid laryngoscopy with stroboscopy a detailed diagnosis can be made. any previous voice disorders and treatment. Assessment Joint ENT/speech and language therapy voice clinics are ideal for professional voice users. Reinke’s oedema (severe). the onset and course of the dysphonia. the therapist’s assessment includes subjective evaluation of: • • • • • • • breathing pattern. working conditions. Where sophisticated assessment facilities are not available. Sulcus vocalis. increases compliance and motivation in therapy. which allow the dysphonia to be repeatedly analysed in terms of physical and acoustic parameters.e.SPEECH THERAPY IN NON-MALIGNANT VOICE DISORDERS 309 • • • • • Occult cysts. • for collection of data for comparative studies and for research and audit purposes. articulation. Speech and language therapy assessment commences with an in-depth case history which highlights factors for therapy planning. e. This facility helps reduce anxiety. palpatory assessment of laryngeal and pharyngeal tension. relationship problems. Objectives for therapy together with an estimated number of sessions required are then set and agreed with the patient.The laryngograph waveform gives quantitative and qualitative information about the closed phase of the vocal cord vibratory cycle. • as a therapy tool to provide instant visual feedback to the patient. have a clear understanding of the diagnosis and try some therapy techniques on camera with clear visual feedback. dynamic range (volume). the frequency range used and a percentage irregularity measure (a measure of the periodicity of vibration. These objective measures can be used: • to provide a baseline before treatment (voice therapy or surgery) and to allow objective evaluation of improvement after treatment. habitual misuse patterns. traumatic life events. i. Traditional assessment is supplemented with objective analysis of pitch. e. Some specialist clinics now have access to instrumentation such as PCLX laryngograph. the mode frequency. quality.g. which correlates with perceived hoarseness). Laryngeal papillomata. a profile of how the voice is used. More time is allocated to each appointment. phonation: habitual pitch and range. questionnaire for patient’s own evaluation of problem. fibrous nodules.g.

yawn-sigh. therapy has to be tailored to the individual. Journal of Speech. When the healthiest possible voice has been achieved the therapist may refer to a singing teacher. Organic changes to the vocal cords often lead to maladaptive patterns of voice use which may persist post-operatively and lead to further problems. Further reading Ramig LO. sex. whose role is to develop technique and advise on singing style. the Accent method. Language & Hearing Research. • a psychotherapeutic approach aimed at releasing anxiety. Postoperative voice therapy is advisable in most conditions. etc. resonance. acoustic. e. 41:101–116. Seminars in Speech Language. Verdolini K. A study of the effectiveness of voice therapy in the treatment of 45 patients with nonorganic dysphonia. Occasionally group therapy may be appropriate. 11:297–309. 1998. general health. Treatment efficacy: voice disorders. attitude to problem and communication requirements. Therapy may include the following approaches: • • • • manipulation of the affected musculature. nasalizing. culture occupation. Carding PN. and the patient has to bring previously automatic activity under conscious control in order to change it. The aim is to change behavioural patterns—to disrupt unhealthy motor engrams for voice and speech and establish and habituate healthy patterns. Journal of Voice. in which separate features are not directly remedied but improve once a physiologically sound pattern of phonation is achieved. fears. Docherty GJ. e. Hillman RE. However therapy is tightly constrained in that techniques must be easy to teach and easy to learn and beneficial effects must be obvious in order to reinforce learning and maintain motivation (Casper. This is not a simple process as there is limited kinaesthetic and proprioceptive feedback from most of the larynx and vocal tract. where patients with similar disorders and a background share common treatment needs. Accurate diagnosis and management of voice problems takes account of laryngological. Voice therapy aims to release the natural voice and/or develop and refine control of specific aspects of voice production to achieve maximum vocal efficiency. 1995). . even if it is not suspected that vocal misuse and abuse was the cause of the problem. which create tension leading to phonation problems. 1990. Voice therapy with singers involves both speaking and singing voice and generally a programme of therapy helps to achieve an easy natural voice without strain. and palpatory case history findings. deep relaxation techniques.g. programmes of therapy in which specific aspects of voice are worked on separately. 1999. taking into account the patient’s age. humming. Although there are fundamental principles of therapy for a given disorder. Horsley IA. use of facilitation techniques e. The efficacy of speech and language pathology intervention: voice disorders. or holistic programmes may be employed. perceptual.310 OTOLARYNGOLOGY Therapy The improved understanding of how phonation is affected by muscle tension imbalance has enabled the development of techniques to elicit specific muscle set responses. intelligence.g. pitch. 13:72–104.g.

Nasal. • Trauma • Inflammatory Septal haematoma and secondary abscess. dentigerous and mucous cysts. External nasal deformity secondary to craniofacial abnormality. septal and midfacial fracture. Wegener’s granulomatosis. Macroglossia. Acquired. nasoalveolar. Infective acute and chronic rhinitis. Dermoid. Meningocele. especially Treacher Collins syndrome. Stertor Aetiology 1. • Nose Choanal stenosis or atresia. Ludwig’s angina. encephalocele. . Acute epiglottitis. Lingual thyroid and thyroglossal cyst. • • Nasopharynx Oropharynx 2. Congenital (present at birth). especially Apert’s syndrome and Crouzon’s disease. Acute and chronic adenoiditis. most frequently in those with Down’s syndrome. especially secondary to infectious mononucleosis. Parapharyngeal and retropharyngeal abscess. meningoencephalocele.STRIDOR AND STERTOR Definitions • Stertor is noisy breathing caused by partial obstruction of the respiratory tract above the larynx. • Stridor is noisy breathing caused by partial obstruction of the respiratory tract at or below the larynx. Craniofacial abnormality. Micrognathia secondary to a craniofacial abnormality. Acute tonsillitis.

cystic hygroma. nasal T-cell lymphoma. Stridor Aetiology 1. central respiratory arrest (in the first 3 months of life neonates are obligatory nasal breathers). an intercurrent URTI or if trauma has occurred. web. Subglottis Web.312 OTOLARYNGOLOGY • Foreign body • Allergy • Neoplasia Allergic rhinitis. A full history should ascertain time of onset. Malignant. stenosis. simple nasal polyps. Treatment Treatment depends on the cause. aggravating and relieving factors. tracheo and bronchogenic cyst. In a child it is important to extend the neck to prevent the retropharyngeal soft tissue causing a pseudo-mass. symptom progression. oropharyngeal and nasopharyngeal squamous cell carcinoma. . • Trachea and bronchi: Web. and acute total airway obstruction. saccular cyst. Glottis Web. Complications These are directly related to the airway obstruction and include right ventricular failure and pulmonary hypertension (sleep apnoea). stenosis.g. Benign. progression and severity of the stertor and on whether it is causing complications (see Related topics). whether there is sleep apnoea. throat (contraindicated in acute epiglottitis) and neck. haemangioma. e. angiofibroma. • Larynx: Supraglottis Laryngomalacia. Congenital. vocal cord paralysis. Examination of the nose. Clinical features Stertor is usually inspiratory but the accompanying features are diverse and depend on the cause.g. antrochoanal polyp. Investigations A lateral soft tissue neck radiograph or an MRI scan may be indicated to show the site of airway obstruction. compression from vascular and other mediastinal tumours. Angioneurotic oedema of the floor of mouth. temperature. respiratory rate and blood pressure may all be necessary. e. pulse. tracheomalacia.

Therefore if the history suggests there may be an aspirated foreign body then bronchoscopy is indicated even with a normal chest radiograph. This will usually allow a confident or a working diagnosis to be made. Investigations A lateral soft tissue neck and chest radiograph. laryngeal or bronchial squamous cell carcinoma. Rigid endoscopy is still the gold standard of investigation as it allows the most complete examination of the aerodigestive tract. 108:378–383. Treatment This depends on the diagnosis and the severity of symptoms (see Related topics). Clinical features Typically. Further reading Zerella JT. 1998. radiographs may be normal. Angioneurotic oedema of the larynx or trachea. . Benign. tracheal. passive opening occurring on expiration. diphtheria. Extrinsic allergic alveolitis. acute laryngotracheobronchitis. A full history combined with examination of the nose. For certain conditions.STRIDOR AND STERTOR 313 2. Quanounou S. Foreign body aspiration in children: value of radiography and complications of bronchoscopy. Malignant. Utility of radiographs in the evaluation of pediatric upper airway obstruction. Dimler. 1999. Immediate treatment or appropriate investigations can thus be instituted. Tracheal and main bronchial airway obstruction causes stridor because of turbulence of air flowing through a narrow but rigid airway that doesn’t collapse. In the smaller bronchi and bronchioles obstruction accentuates the physiological constriction occurring in expiration to cause an expiratory wheeze.g. throat and neck is indicated if circumstances permit. Walner DL. Journal of Pediatric Surgery. McGill LC. Acute laryngitis. It may be inspiratory.g. iatrogenic (intubation and surgical). 33(11): 1651–1654. Acquired. e. 87% had more than one abnormality including 33% with gastro-oesophageal reflux (see Related topics). laryngeal papillomatosis. Pippus KJ. the negative inspiratory intralaryngeal pressure indrawing the supraglottic soft tissues. blunt and sharp external. bronchial and external compression from an oesophageal foreign body. Annals of Otolaryngology. or a CT scan of the larynx and lungs may be appropriate. A representative biopsy of a laryngeal or infralaryngeal mass may be indicated. Cotton RT. It must be emphasized that in children with a bronchial foreign body. e. In one study of stridulous neonates. including foreign body aspiration and innominate artery compression chest radiographs are very good at suggesting the correct diagnosis (86% in one study). • • • • • Trauma Inflammatory Foreign body Allergy Neoplasia Thermal and chemical. Donnelly LF. expiratory or biphasic. Laryngeal. supraglottic stridor is inspiratory.

p.314 OTOLARYNGOLOGY Related topics of interest Paediatric airway problems. p. Nasopharyngeal neoplasm. p. 170. p. Foreign bodies. p. p. . p. Nasal granulomas. 174. Laryngectomy. p. Nasal malignancy. Adenoids. Laryngeal carcinoma. 103. 143. p. 138. Oropharyngeal carcinoma. 232. 203. 180. 8.

Nearly all those with a .g. cholesterol granulomas.SUDDEN HEARING LOSS Sudden hearing loss is a significant subjective decline in the hearing acuity occurring either instantaneously or progressively over minutes or hours. Usually only one ear is affected and the aetiology often never identified.g. loop diuretic and chemotherapetic drugs. from wax or a foreign body. from a direct blow. latrogenic.g. Conductive causes • • • • External ear canal occlusion e. Autoimmune inner ear disease. It can be classified into conductive and sensorineural causes. in particular aminoglycoside antibiotics. latrogenic Serous and purulent labyrinthitis. Viral e. Menière’s disease (primary endolymphatic hydrops) and secondary endolymphatic hydrops (which may cause Menière’s syndrome). congenital dermoids and meningiomas. Ototoxic drugs. Ear trauma. Sensorineural • • • • • • • • • • • Idiopathic. Central causes e. in particular transverse fractures.g from blast trauma or barotrauma. following a brain stem cerebrovascular accident. Infection e. Temporal bone fractures. otitis externa.g. Causes of perilymph fistula including round window rupture e. beta-blocker. Clinical features In subjects with an identifiable cause of a sudden hearing loss the diagnosis is usually made from a thorough otological and neurological history. acoustic neuromas. acoustic or barotrauma (see Related topics of interest). Cerebellopontine angle tumours e. measles and mumps virus. examination and relevant special investigations.g. non-steroidal antiinflammatory. acute otitis media or chronic otitis media.

. Management All patients with a sudden bilateral sensorineural hearing loss should be admitted to hospital for several reasons: (a) Close monitoring of the hearing by pure tone and speech audiometry is possible and desirable in order to determine whether the hearing is stable. p. Those with a sudden unilateral hearing loss will have less of a disability and handicap. Further reading Byl F. p. blood viscosity lowering substances (e. antioxidants combined with steroids. dextran 40). p. 1983. (c) To provide rehabilitation in the form of (i) counselling from a hearing therapist. steroids. 118:737–738. MRI imaging. 5. Labyrinthitis. 1998. Management of sudden deafness. p. telephone bell. and do not require such urgent rehabilitation. It is generally agreed by those who advocate such treatment that it should commence as early as possible after the onset of the hearing loss and certainly within the first few days of symptoms.g. 218. Maffee M. Fitzgerald DC & Marks AS. 38. Ototoxicity. Chronic otitis media. 1986. viral titres (two sets. 91:3–8. 228. improving or declining. Kumar A. 1. six weeks apart) and syphilis serology in an effort to make a diagnosis. p. anticoagulants (e. 244. Otolaryngology and Head and Neck Surgery. (ii) hearing aid and accessory aid provision (for example amplification of the TV. Maudelonde C. Menière’s Disease. Related topics of interest Otological aspects of head injury. betahistine). p. Sudden hearing loss: eight years experience and suggested prognostic table. about the same as those who spontaneously recover with no treatment.g. The Laryngoscope. p. The Laryngoscope.316 OTOLARYNGOLOGY sudden conductive hearing loss will have a definitive diagnosis made but 60% of the sensorineural group will eventually be labelled as idiopathic of which 60% will recover spontaneously. trauma. Most treatments report a response rate of 60%. 134. 1984. This will provide a hearing prognosis and enable the patient’s disability and handicap to be assessed.g.M. and antibiotics is empirical. Perilymph fistula. telephone receiver and door bell). 96:14–18. Otolaryngology Head and Neck Surgery. Acoustic neuroma. Fisch U. p. heparin). Treatment of the idiopathic group with vasodilators (e. Acute otitis media. MRI in sudden sensorineural hearing loss. 94: 647–661. (b) To allow rapid performance of relevant special investigations which may include electric response audiometry. 167. Unilateral sensorineural hearing loss: an analysis of 200 consecutive cases. purulent labyrinthitis) dictates and they can be investigated as an out-patient.g. As a general rule they do not require admission into hospital unless the aetiology (e.

and recurrent nodular. nodular.C. hypothyroidism and hyperthyroidism. post-treatment of thyrotoxicosis with radio-iodine. Benign and malignant. Hypothyroidism may be congenital or acquired. multinodular. De Quervain’s. multinodular. Reidel’s thyroiditis. on which fine needle aspiration cytology can be performed. Although thyroid nodules are common it is important to remember that thyroid cancer is extremely uncommon. syphilis. 1. Within this group. Multinodular goitre can be associated with iodine deficiency which is endemic in patients living at high altitude such as the Alps or Himalayas. These may be both physiological and pathological. or . and recurrent nodular. The differential diagnosis of the solitary thyroid nodule (apart from a colloid nodule) includes a follicular adenoma. Patients with hypothyroidism may or may not have a simple goitre. These are thyroid goitre. It is important to have as much information as possible on any patient prior to surgery. thyroid cyst or carcinoma. The causes of pathological goitres include iodine deficiency. Rarely it is associated with inherited dyshormonogenesis such as Pendred’s syndrome (which is the association of congenital hypothyroidism with high tone deafness). This will also assist in delineation of the most prominent nodule. pregnancy and with the contraceptive pill. amyloid. Diffuse. it is estimated that up to 15% of the population have a goitre. An ultrasound scan will help confirm the diagnosis. Nodular goitre may be solitary or multinodular. with an incidence in the UK of between 1–2 per 100 000. The commonest way for cancer to present is as a solitary thyroid nodule. approximately 8% have nodular thyroid disease of which 50% are solitary. Simple (non-toxic) goitre. The majority of patients with multinodular goitre are euthyroid. Physiological goitres include puberty. HIV and lithium. clinical oncologist and endocrinologist. Acquired hypothyroidism is usually idiopathic or due to surgical ablation of the gland. These cases are probably best dealt with by a multidisciplinary team including a head and neck surgeon.THYROID DISEASE—BENIGN J. Classification of goitre • Simple (non toxic) • Toxic • Inflammatory • Neoplastic • Rare goitres Diffuse. Hashimoto’s. The benign nature of the disease may be confirmed in this way. nodular. In the United Kingdom. Patients with thyroid goitre are the most important from a surgical standpoint as it is this group that is often referred to ENT surgeons by general practitioners for primary management.Watkinson Benign thyroid disease can be analysed from three different aspects which are often interrelated. TB. The former is usually due to congenital absence or atrophy of the thyroid and untreated leads to cretinism.

Inflammatory goitre. Toxic goitre (hyperthyroidism). Because of this. Recurrent thyrotoxicosis is treated on its merits. (a) Hashimoto’s thyroiditis. Patients with thyrotoxicosis usually either have Graves disease or a solitary toxic nodule. Patients who have solitary toxic nodules are usually best dealt with surgically. This can be a benign adenoma or malignant tumour (see Related topic of interest). For example sarcoidosis. Graves disease is caused by circulating thyroid stimulating immunoglobulins (IgG) which bind to thyroid stimulating hormone receptors (TSH receptor) to increase thyroid hormone production. This is most common in late middle-aged women. but may become hypothyroid as the disease progresses. together with those who have significant eye signs or who request surgery. Once the diagnosis is made. amyloid. atrophy and regeneration of the thyroid. . normal free T4). They cause lymphocyte infiltration. and the rise in T4 is often associated with atrial fibrillation.318 OTOLARYNGOLOGY Hashimoto’s thyroiditis. Rarely surgery may be required for an enlarged gland causing obstructive symptoms or when there is a fine needle aspiration cytology result that necessitates surgery. then treat with T4 (100 µg/day) if antibodies are positive. an operation with a ‘near total’ or ‘total’ thyroidectomy is an alternative option. These patients are at a high risk of subsequently developing a thyroid lymphoma. Radioiodine can also be used to treat large multinodular goitres in the elderly and infirm. and associated with diffuse swelling and tenderness of the gland. these patients usually have cardiac signs (and not eye signs) and are usually treated medically. Some patients who have had a multinodular goitre for a long time can develop thyrotoxicosis (Plummer’s disease). 4. The gland is usually firm. 5. if there are convincing symptoms or a past history of radioiodine treatment. Antibodies are directed against thyroglobulin and/or microsomal peroxidase. Miscellaneous goitres. Neoplastic goitre. Many patients (whatever their treatment) will be hypothyroid post-treatment and will be on long-term thyroxine replacement therapy. This is a flu-like illness. Graves disease may also be associated with signs of vitiligo. Hyperthyroidism is usually treated either medically using tablets (carbimazole or Propylthiouracil) or with radioiodine. pretibial myxoedema and other autoimmune disorders such as pernicious anaemia. These immunoglobulins are usually associated with thyroid eye disease which is caused by a specific antibody called exophthalmos producing substance (EPS) which targets retro-orbital tissue to cause oedema of fat and muscle. and ultimately a goitre. patients should be treated with thyroxine suppression and have thyroid function tests once a year. Initially patients are hyperthyroid. There is usually both a transient hyperthyroidism and production of auto-antibodies. Treatment is with thyroid hormone replacement. These patients are often elderly with co-existent morbidity such as ischaemic heart disease. HIV infection. This is thought by some to signify a fibrotic reaction to an underlying carcinoma or lymphoma. tuberculosis. but rubbery. (b) De Quervain’s thyroiditis is secondary to an acute viral infection. About 50% of patients will relapse following medical treatment. but may require further treatment with either the same or another modality. 3. 2. (c) Riedel’s thyroiditis is rare and associated with a woody hard. The starting dose is usually T4 100 µg/day. when good shrinkage is achievable. irregular thyroid gland which histologically shows marked fibrosis. In these patients. In the presence of subclinical hypothyroidism (high TSH > 10 mU/1. sometimes tender.

difficulty in swallowing and breathing and in those patients undergoing surgery. sulphonylureas. A chest X-ray may show tracheal deviation. It may also be used to evaluate complex cysts and can distinguish and identify purely cystic nodules. hyperthyroid or hypothyroid. Treatment The indications for surgery are: • • • • Suspected malignancy. Truly functioning nodules (hot) are highly unlikely to be malignant. patients may be euthyroid. Ultrasound may be helpful in measuring tumour size. the visceral compartment of the neck. the likelihood of a solid cold nodule being malignant rises to about 50%. The latter is suspected from dullness to percussion over the manubrium. e. Examine the rest of the neck for nodes and perform indirect or fibreoptic laryngoscopy to check the mobility of the vocal cords. carcinoma. a serum calcium and calcitonin may be appropriate. pulmonary metastasis or associated co-morbidity but the best way to assess upper airway obstruction is with a flow loop. . position and any retrosternal involvement. diagnosing multinodular goitres and excluding contralateral disease. ultrasound cannot reliably distinguish between benign and malignant disease. It is important to confirm that the swelling moves with swallowing and to note its size. Thyrotoxicosis.g. the neck for nodes. a cyst or a dominant nodule in a non-palpable multinodular goitre and the likelihood of malignancy in a truly solitary ‘cold’ nodule is between 10% and 20%. and whole body staging for lymphoma. The diagnostic strategy for evaluating the thyroid nodule is shown below. In addition. Cosmetic reasons. These clinically solitary nonfunctional nodules may be an adenoma. the abdomen. Depending on the history. all euthyroid patients should have fine needle aspiration cytology performed and a vocal cord check is advised in those with any voice change. cheap and reliable with a diagnostic accuracy of approximately 90% and is therefore the initial investigation of choice for a solitary thyroid nodule. mediastinal extension or lymphadenopathy. the chest. The goitre may produce discomfort on swallowing. However. or is ‘cold’ (and therefore not functioning). More than 90% of lesions identified with scintigraphy will not concentrate the radionuclide and therefore will appear ‘cold’. or stridor (implying tracheal compression). If a cyst has been excluded on ultrasound. Investigations All patients with a goitre should have their thyroid function and thyroid antibody status checked. Tracheal or oesophageal compression. Anatomical imaging with CT or MRI is useful to assess both thyroid lobes. Only rarely is a cyst associated with a thyroid cancer. the mediastinum.THYROID DISEASE—BENIGN 319 Clinical assessment Depending on the cause and duration of the goitre. Radionuclide scintigraphy using I123 can be used to identify whether a nodule is ‘hot’ (takes up isotope) and therefore is functioning. A drug history is important because some are goitrogens. dysphagia (implying oesophageal compression). Fine needle aspiration cytology is safe.

Hemithyroidectomy (total lobectomy). A ‘near total’ thyroidectomy is a total lobectomy and the isthmusectomy with removal of more than 90% of the contralateral lobe and is often done to preserve blood supply to parathyroids on one side. Subtotal thyroidectomy. A . A lumpectomy is removal of the nodule alone with minimal surrounding thyroid tissue. while a total lobectomy completely removes one thyroid lobe with the isthmus. A subtotal thyroidectomy is bilateral removal of more than one half of the thyroid gland on each side plus the isthmus and is rarely performed nowadays. Near-total or total thyroidectomy.320 OTOLARYNGOLOGY Types of surgery The following operations can be performed on the thyroid gland: • • • • Lumpectomy.

(b) Tracheomalacia (uncommon). (d) Pneumothorax. surgery for large goitres and can be reduced when operations are performed by an experienced surgeon and by use of a nerve stimulator. (d) Poor scar. but permanent damage is treated with replacement therapy using alphacalcidol. (a) Haemorrhage which can be immediate or delayed. 1. Hormonal. 2. (a) Recurrent laryngeal nerve damage. The incidence of damage to the recurrent laryngeal nerve is approximately 2%. The incidence is unknown but is increased in surgery for cancer. (b) Damage to the external branch of the superior laryngeal nerve.THYROID DISEASE—BENIGN 321 ‘total’ thyroidectomy is removal of both thyroid lobes and the isthmus with preservation of the parathyroids and a completion thyroidectomy is a subsequent procedure to convert a lesser operation into a near total or total thyroidectomy. (b) Thyroid crisis (acute exacerbation of thyrotoxicosis). (a) Tetany (hypoparathyroidism which is secondary to parathyroid removal or bruising). Complications of the wound site. This may recover and if so is covered with calcium replacements. Injury to related anatomical structures. (c) Wound infection. the minimum operation that should be done on the thyroid gland is a total lobectomy. Follow-up and aftercare In those patients who have had a hemithyroidectomy. This is particularly common in the elderly and in those who have positive thyroid antibodies. It can cause tracheal compression. Complications of thyroidectomy As well as the hazards of any surgical operation there are specific potential local and general complications of thyroidectomy. (c) Hypothyroidism (secondary to extensive removal of thyroid tissue). Treatment is with evacuation. If there is still evidence of subclinical hypothyroidism. It is related to the experience of the surgeon and increased for operations involving malignancy and for revision surgery. Patients who have had a ‘near total’ or ‘total’ thyroidectomy usually require immediate Thyroxine replacement therapy . In general. (c) Damage to the trachea. thyroid function is checked at 6 weeks to check the contralateral lobe is functioning normally and if not a further blood test is done at 3 months. patients may well require long term thyroxine replacement therapy. (d) Late recurrence of thyrotoxicosis (incomplete removal of the toxic gland to include the pyramidal lobe) 3.

p. Further reading Drury PL. 798–809. 1990.322 OTOLARYNGOLOGY and all patients following thyroidectomy should have a vocal cord mobility checked so that the true incidence of cord paresis for one particular surgeon can be documented. Corrected serum calcium levels should be performed routinely 24 hours post-operatively to counteract iatrogenic hypoparathyroidism. Related topic of interest Thyroid disease—malignant. 322. 2nd edn. Clinical Medicine. In: Kumar PJ. . London: Baillière Tindall. Clarke ML (eds). The thyroid axis.

as mixed papillaryfollicular carcinoma or as the follicular variant papillary carcinoma. Its various types are: • Minimal (or microcarcinoma): less than 1 cm. Papillary adenocarcinoma (along with follicular adenocarcinoma) is a differentiated thyroid cancer and accounts for 80% of thyroid malignancy. Follicular adenocarcinoma occurs in older age groups between 40 and 60 years and is seldom seen under the age of 30. Genetic predisposition. 2. These are: • • • • • • • Natural diet deficient in iodine. While papillary carcinoma can be identified on . on occasion. It is associated with a high incidence of cervical lymphadenopathy which may. • Intrathyroidal: greater than 1 cm. Papillary thyroid cancer either exists in a pure papillary form. A history of previous ionizing radiation. • Extrathyroidal: extending beyond gland capsule and/or lymph node metastases.C. 1. which are usually to the lungs.Watkinson Aetiology Carcinoma of the thyroid gland is not common. Several factors are now known to be important in its causation. It usually presents as a solitary thyroid nodule. Male gender. History of previous thyroid cancer. be the only initial presenting feature. Classification There are various types of thyroid tumours and these are shown in Table 1 below. Less than 10% will have distant metastases. It is less common than papillary thyroid cancer (10% of all thyroid malignancy) and usually presents as a solitary thyroid nodule or occasionally with either distant bony metastases or cervical node involvement (about 10%).THYROID DISEASE—MALIGNANT J. Increased secretion of thyroid stimulating hormone. Follicular adenocarcinoma. Chronic lymphocytic thyroiditis. but is often multicentric. Papillary adenocarcinoma. It occurs in all ages and is the commonest type of thyroid cancer in children.

Once the diagnosis is made. The clinical presentation can be identical to anaplastic carcinoma and both these conditions should be excluded from each other by open biopsy. which has a good prognosis. Primary thyroid lymphomas are uncommon and account for fewer than 5% of all lymphoma cases. Therefore. 3. a tracheostomy may be required and most patients are dead within one year. patients require formal staging and treatment is with radiotherapy plus or minus chemotherapy. and cervical node metastases are common. Anaplastic carcinoma. The autosomal dominant MEN IIa is associated with phaeochromocytomas (10%) and parathyroid hyperplasia (60%). as familial non MEN disease or in sporadic form. Treatment of anaplastic carcinoma with radiotherapy is often ineffective. These tumours are common in elderly women and many are superimposed on a long standing multinodular goitre.324 OTOLARYNGOLOGY Table 1. In patients with MEN. They present with rapid thyroid enlargement. a diagnostic thyroid lobectomy is usually required. They usually present as a rapidly increased swelling of the neck in an elderly woman and there is often a history of Hashimoto’s thyroiditis. Genetic screening is now possible for familial disease using the ret proto-oncogene. it is frequently bilateral (90%) and multifocal. are aggressively malignant and rapidly invade surrounding structures. Its histology comprises of swarms of small cells and can be difficult to distinguish from lymphoma. and CD4/CD8 lymphoid cell markers is required. immunohistochemical staining for cytokeratin squamous cell marker. phaeochromocytomas and Marfan’s syndrome. . Therefore. Lymphoma. They have a bad prognosis. It may occur as part of the multiple endocrine neoplasia (MEN) syndrome. 4. Classification of thyroid tumours fine needle aspiration cytology. it is not possible to diagnose a follicular carcinoma using this technique since it cannot distinguish an adenoma from a carcinoma. Medullary thyroid carcinoma. Medullary cancers arise from the parafollicular or C cells which secrete calcitonin and this can be a valuable tumour marker. 5. MEN IIb is medullary carcinoma associated with mucosal neuromas. This condition accounts for about 5% of all cases of thyroid malignancy.

Tumour 1 cm-4 cm. midline. The experience of the surgeon is also important. Management There are a number of treatment modalities for thyroid malignancy: . All categories may be subdivided into (a) solitary tumour. An ultrasound may be useful to measure the size of the primary tumour. Many will present with a solitary thyroid nodule so will have had FNAC. Patients over 45 do worse and women do better than men. Tumour size is important as is tumour histology with papillary tumours doing better than follicular and both of these do better than medullary. Metastases in bilateral. Prognostic factors There are a number of prognostic factors associated with differentiated thyroid cancer and these are listed below: • • • • • • • • Age. local invasion or distant spread. Treatment with postoperative radio-iodine. Tumour of any size extending beyond the thyroid capsule. Staging T1 T2 T3 T4 Tumour < 1 cm. Tumour > 4 cm. or contralateral cervical or mediastinal nodes. Tumour histology. Sex. Thyroid hormone manipulation. The presence of nodal metastases. The extent of surgery is important with survival rates being the best in a group of patients who have total thyroidectomy and radio-iodine ablation. (b) multifocal tumour N0 N1 N1 N1b No regional lymph node metastases. Extent of surgery. Nodal metastases carry a worse prognosis in the elderly and patients do worse in the presence of local or distant spread. to assess the contralateral lobe and to facilitate FNA in certain cases. Patients with advanced disease should be imaged with CT or MRI. Metastases in ipsilateral node. Whole body staging for lymphoma is done with CT. Tumour size.THYROID DISEASE—MALIGNANT 325 Investigations All patients should have thyroid function tests and thyroid antibodies. Regional lymph node metastases.

As the tumour size increases. Follicular adenocarcinoma For follicular carcinoma. Those tumours greater than 1 cm and those associated with cervical or distant metastases are high risk. Nodal and distant metastases. thyroid hormone suppression and serial thyroglobulin measurements.326 OTOLARYNGOLOGY • • • • • Surgery. However. There is a risk that the tumour will be multicentric. the jugular vein is palpated and any suspicious nodes in levels II to V and VII are sent for frozen section and. it is reasonable after discussion with the patient to offer a conservative approach for tumours less than 3 cm in size when age and gender indicate a low risk patient. if involved. Clinically palpable disease requires at least a selective neck dissection involving these levels. This allows a surgical treatment strategy as shown in Table 2. Radio-active iodine. In these cases it seems entirely reasonable to advocate a conservative approach with hemi-thyroidectomy. Stage and Histology (GASH) is shown below: • • • • • Gender. Chemotherapy. Modified radical or radical neck dissections may be required. Treatment of differentiated thyroid tumours based on risk stratification A risk stratification based on Gender. Tumour histology. All patients with differentiated thyroid cancer require a level VI dissection as part of the total thyroidectomy. Treatment of the T2 lesion (1–4 cm) remains controversial but again following thyroid lobectomy for a suspicious FNA based on current data. External beam radiotherapy. Hormonal manipulation. some may prefer to advocate total thyroidectomy and radio-iodine ablation. survival rates fall and certainly any patient with a tumour which measures greater than 3 cm or one with local or distant spread should be treated with total thyroidectomy and radio-iodine ablation. Papillary adenocarcinoma The treatment of this cancer is with surgery and the outlook is excellent. . At the time of surgery. Data from the Mayo clinic shows that patients who have tumours which measure less than 1 cm in size have an excellent prognosis and a 99% chance of living 20 years (the T1 lesion). distant spread is more common so that tumours less than 1 cm which exhibit minimal invasion can be treated with conservative hemithyroidectomy but the rest (which will be the majority) require total thyroidectomy and radio-iodine ablation. Age. Patients can be divided into high risk or low risk (females under 45 are low risk) and there are low risk and high risk tumours (low risk tumours measure less than 1 cm in size). Age. Tumour size. a selective neck dissection of levels II to V or VII is carried out as appropriate.

Any uptake in the neck requires a therapy dose of I131. ButterworthHeinemann.THYROID DISEASE—MALIGNANT 327 Table 2. Protocols are available and patients are put on suppressive doses of T4 and an I131 whole body diagnostic scan carried out after ablation to confirm whether or not the treatment has been successful. 4th Edition. Identify and attempt to preserve both recurrent laryngeal nerves. The strap muscles may need to be divided. Vol. Visceral extension into the larynx or pharynx may require extensive surgery. Further reading The management of the solitary thyroid nodule: a review by RM Walsh. A total thyroidectomy is done with a level VI dissection and any palpable nodal disease requires modified radical or radical neck dissection. 2000. Any involved nerve should be resected. Parathyroid preservation is important. Tumours of the thyroid and parathyroid glands. Effective Head and Neck Cancer Management. Second Consensus. It is usually possible to perform conservative surgery preserving at least the accessory nerve as well as sometimes both the sternomastoid muscle and the internal jugular vein. In: Clinical Otolaryngology. 1999. JC Watkinson & J Franklyn. radio-iodine ablation of the residual normal thyroid tissue can be performed in the post-operative period after allowing TSH levels to rise. British Association of Otolaryngologists. 2000. Major vessel involvement is uncommon but usually indicates inoperability. . 24:388–397. Medullary thyroid cancer Treatment for this is surgical. Access to the mediastinum may be required. Level VI dissection should always be done with a total thyroidectomy. Total thyroidectomy for cancer The following points are important when performing the above operation: • • • • • • • • Adequate access is required via the appropriate incision. In: Stell and Maran’s Head and Neck Surgery. Head and Neck Surgeons. The treatment of anaplastic carcinoma and lymphoma has already been discussed. Usually level I does not need to be dissected in the untreated neck. Surgical treatment of differentiated thyroid cancer Following total thyroidectomy. Wilson J (ed).

Epidemiology Tinnitus is a common experience with up to one third of the adult population experiencing it at some time in their life. Hyperacusis (as distinct from recruitment) is found as an associated symptom in about 40% of tinnitus sufferers. (b) This signal will undergo extensive auditory processing before it is perceived as tinnitus. There are several hypotheses which attempt to explain these phenomena: 1. Central processing. There is some evidence that tinnitus is associated with an increase in the spontaneous firing rate of auditory nerve fibres. 3.TINNITUS Definition Tinnitus is the sensation of sound not brought about by simultaneously externally applied mechanoacoustic or electrical signals. Altered auditory firing rate. Less than 1% of the adult population have tinnitus of sufficient severity to seriously affect their quality of life (although up to 8% may seek medical advice about it). may cause damage to the myelin insulation between axons in the peripheral auditory system. A ‘neurophysiological’ model has been developed which suggests three phases in the aetiology of tinnitus: . leading to ‘cross-talk’ between them and thus to phase locking of spontaneous neural activity. Hyperacusis can be defined as an undue sensitivity and distress to everyday sounds that would not normally trouble a ‘normal-hearing’ individual. Pathophysiology The cause of tinnitus is not known. Hence the association with a high tone hearing loss. The prevalence of tinnitus increases in association with a high frequency hearing loss although the association between severity of tinnitus and degree of hearing loss is very weak. experienced subjectively as tinnitus. Recent years have seen an increased appreciation of the role of central signal processing in tinnitus perception. by any mechanism. It has been postulated that damage to the cochlea. 2. Cross talk. This definition excludes vascular sounds and bruits. In developing an understanding of tinnitus mechanisms two points should be borne in mind: (a) There is a generated potential somewhere in the auditory system.

and the great majority of tinnitus sufferers have some measurable hearing loss. Clinical assessment From the patient’s history confirm that the patient is actually suffering with tinnitus and determine the character of the sound (intermittent or constant. • A pure tone audiogram is essential to document any hearing loss. Investigations 1 . Almost every ear disease and cause of deafness can be associated with tinnitus. cardiac failure). Effects on sleep. Noise induced hearing loss seems to be particularly frequently associated with tinnitus as does Menières disease. and finally. • Detection and then (usually negative) perception. . It has become clear in recent years that the ‘problem’ of tinnitus relates far more to the individual’s psychological response to the abnormal tinnitus signal than to the signal itself. 2 . Local causes.TINNITUS 329 • Emergence of the signal (perhaps due to local cochlea pathology). Usually the pitch of the tinnitus is found to be at or around the frequency of the maximal hearing loss and the loudness is usually within 15 dB of the patient’s pure tone threshold at that frequency. vascular malformations and exceptionally loud spontaneous otoacoustic emissions. • Persistence—due to autonomic arousal. Objective tinnitus may be found in palatal myoclonus. • Loudness discomfort levels are useful if there is any co-existent hyperacusis. Audiometric investigations. Neurological conditions (multiple sclerosis. It is also important to establish how much trouble the patient is having because this will dictate whether and how much treatment is necessary. MRI scanning will then be required. These include cardiovascular disease (hypertension. pulsatile or non-pulsatile). A full ENT and cardio-vascular examination should be performed to ensure the patient is not hearing transmitted sounds or does not have a potentially remedial causes of tinnitus. Associated conditions 1. These tests make the assumption that the characteristics of an external sound can be meaningfully related to those of an internally generated sound. mood and concentration are found most frequently. 2. Unilateral tinnitus may also be the only symptom of an acoustic neuroma. It should be remembered that 10% of acoustic neuromas present with markedly asymmetrical tinnitus. • Tinnitus pitch and loudness matching may be performed. When measured sequentially they can indicate response to treatment. anxiety and negative beliefs. neuropathy) may also lead to tinnitus. There is a consensus that psycho-acoustic tests of this kind give no useful information regarding tinnitus severity nor is there any relationship between perceived loudness of tinnitus and complaint behaviour. a hyperdynamic circulation as in anaemia and fever and drugs (particularly salicylates). There is also evidence of increased central auditory gain in tinnitus sufferers and it may be this phenomena that explains the frequently associated hyperacusis. General causes.

lignocaine. audiologists. lay counselling and relaxation therapy. p. Tinnitus. These are useful for those patients who have a hearing loss. In the absence of a clear diagnosis a full haematological screen to exclude anaemia. • Many other treatments have been tried (e. Management Any underlying remedial cause should be treated first. 1993. • Hearing aids. Hearing aids. Thereafter. In: Scott-Brown’s Otolaryngology. if tinnitus persists. Modern treatment is described as habituation based therapy and consists of two main components: directive counselling and sound therapy. and ideally. ginko biloba amongst others) but success has been limited and adverse effects common. 2. D Stephens (ed). It is thought to act both by reducing the contrast between the tinnitus signal and background noise and improving the plasticity of the central auditory cortex and thereby facilitating a reduction in perception. a clinical psychologist. hearing therapists. Further reading Coles RRA. 254. dyslipidaemias and hypoglycaemia can be helpful. p. hearing aids and/ or white noise generators (WNG) to raise the background ‘sound floor’ and thus reduce the prominence of the tinnitus signal. 6th edn.330 OTOLARYNGOLOGY 3 . broad-band sound. Vol. Objective pulsatile tinnitus may require angiography if a specific vascular lesion is suspected. Related topics of interest Evoked response audiometry. 78. British Journal of Audiology. London: Chapter 18. • A pillow radio or pillow speaker may help the patient get to sleep. • White noise generators (WNG). Butterworth-Heinemann. p. These produce a controllable and more palatable. 27:7–17. 117.g. Access to a local self-help group is useful to provide emotional support. Pure tone audiogram. the increased awareness of the background sound tends to make the tinnitus less apparent. thyroid dysfunction. melatonin. Directive counselling involves explaining the problem. 4 . countering negative beliefs and making efforts to ameliorate the tinnitus sufferer’s reaction to the perception of their tinnitus signal. If an appropriate aid with maximal gain at around the frequency of the tinnitus is fitted. Jastreboff PJ and Hazell JWP. Adult Audiology. Sound therapy or sound enrichment involves the use of background sound. Useful for those with severe tinnitus and a hearing loss. management is best undertaken by a dedicated team comprising otologist. . • Combined hearing aid and WNG unit. These are particularly useful for individuals with a minimal or no hearing loss. A neurophysiological approach to tinnitus: clinical implications. magnetic and ultrasonic stimulation.

There may be trismus and dribbling. They are part of Waldeyer’s ring. white cell count and a throat swab. and it would be prudent to perform a Paul-Bunnell test. The tonsil is enclosed by a fibrous capsule. which is most often a viral infection involving the lymphoid tissue on the posterior pharyngeal wall and may include the tonsil. adenoviruses. . Cases that are referred to hospital are usually more severe. Pain may radiate to the ears or may occur in the neck due to cervical lymphadenopathy. its aetiology and pathogenesis are poorly understood. Streptococcus pneumoniae. Swallowing may be painful (odynophagia) and the patient’s voice may sound muffled. It is regarded as being distinctive from acute pharyngitis. Glandular fever. enteroviruses and rhinoviruses) may be responsible for tonsillitis in up to 50% of occasions. There is some doubt regarding the most common causative organisms in acute tonsillitis. In general practice the clinical features usually make the diagnosis obvious without the need to resort to clinical investigations in the majority of cases. Some children may have abdominal pain and occasionally vomiting. which is a sore throat. a ring of lymphoid tissue consisting of the adenoids. particularly the jugulodigastric nodes. It has been suggested that viruses (e. it is most frequent in child-hood. The ring as a whole is thought to have some protective function as a barrier against infection in the first few years of life. This separates the capsule from the pharyngobasilar fascia covering the superior constrictor muscle that forms the tonsil bed. In many other cases it is felt that an initial viral tonsillitis may predispose to a superinfection by bacteria ( -haemolytic streptococcus. malaise and headache for a day before the onset of the predominant symptom. Acute tonsillitis is an infection which primarily affects the palatine tonsil. Aetiology of acute tonsillitis Although this is a common disease. para-influenza. outside of which is a layer of areolar tissue. leukaemia and diphtheria must always be borne in mind. agranulocytosis. Haemophilus i influenzae and anaerobic organisms). There will be tender cervical lymphadenopathy. The tonsils are found to be hyperaemic on examination with pus and debris in the crypts.TONSIL DISEASES The tonsils are paired secondary lymphatic organs situated on the side of the oropharynx between the palatoglossal (anterior tonsil pillar) and palatopharyngeal folds (posterior tonsil pillar). influenza. the palatine tonsils and the lingual tonsils (which are embedded in the posterior third of the tongue). The main blood supply of the tonsil is from the tonsillar branch of the facial artery. how-ever. presumably because immunity to common childhood organisms has not been fully established. Although the disease is seen in adults.g. Clinical features There may be a prodromal illness with pyrexia.

Fluid replacement and bed rest are ancillary measures in the severe attack. • Acute streptococcal tonsillitis. General. Parapharyngeal. Meningitis. Differential diagnosis of ulceration of the tonsil A working diagnosis can usually be determined from the history and clinical examination. Investigations include a full blood count.332 OTOLARYNGOLOGY Management Even though viruses are implicated as the pathogenic organisms in many cases. • Diphtheria. • Recurrent acute tonsillitis (chronic tonsillitis). 2. Differential diagnosis of unilateral tonsil enlargement • Asymmetry in a patient with recurrent bouts of acute tonsillitis. Local. Ampicillin should never be used to treat acute tonsillitis in case the patient has infectious mononucleosis. . when a generalized maculopapular rash may develop. Infection. Aspirin is contraindicated in children because of the risk of Reye’s syndrome. • • • • Septicaemia. Retropharyngeal. • Acute otitis media. The patient should have paracetamol for analgesia. • Apparent enlargement (peritonsillar abscess or parapharyngeal mass). Complications of acute tonsillitis 1. with erythromycin reserved for those patients allergic to penicillin. • Infectious mononucleosis. it is likely any patient who attends a medical practitioner with the clinical features of tonsillitis will be treated with antibiotics. • Neoplasia (squamous cell carcinoma or lymphoma). Possible causes include: 1. • Severe swelling causing respiratory obstruction. Penicillin V is still the drug of choice. • Abscess formation: Peritonsillar (quinsy). serological tests and biopsy. Acute rheumatic fever. chest radiograph. Acute glomerulonephritis.

Acute infection of the pharynx and tonsils. . Advances in adenotonsillar disease. 6th edn. p. Further reading Hibbert J. Current Opinion in Otolaryngology and Head and Neck Surgery. Other causes. Neoplasm. 1993. 1997. Related topics of interest Adenoids. 333. In: Hibbert J (ed). p. Neck space infection. • Behçet’s syndrome. 5. • Salivary gland tumours (adenoid cystic carcinoma or mucoepidermoid tumour). Blood diseases. Hotaling AJ. 3. 188. Chapter 4. • Squamous cell carcinoma.TONSIL DISEASES 333 • Vincent’s angina. Silva AB. p. 8. 4. London: Butterworths. • Lymphoma. • Acquired immunodeficiency syndrome (AIDS). Tonsillectomy. • Leukaemia. • Aphthous ulceration. 2. 1:177–184. Scott-Brown’s Otolaryngology. Vol. • Agranulocytosis.

• Suspected neoplasm (unilateral enlargement or ulceration). During certain epidemics (e. access to glossopharyngeal nerve or styloid process). but surgery should be delayed until the particular problem is resolved. . Cleft palate. In some cases the decision to proceed with surgery should be reconsidered in the context of the potential problems. • Gross enlargement causing airway obstruction (sleep apnoea syndrome). Oral contraceptives. Although it is felt that the risk is extremely small. etc) should be disposable. Complications of tonsillectomy 1. scissors. Peroperative. five per year. polio). Tonsillectomy and CJD Concerns have been expressed about the potential for contamination of tonsillectomy instruments with ‘prions’ and subsequent development of Creutzfeldt Jakob disease (CJD). steps have been taken to minimize it. As a rule of thumb these episodes should last 5 days or more.g. • Part of another procedure (UVPP. for at least 2 years. • • • • • Recent episode of tonsillitis or upper respiratory tract infection (within 2 weeks). Current advice is that instruments which are in intimate contact with the tonsil (dissecting instruments. Bleeding disorder. (Surgeons differ in the definition of this.TONSILLECTOMY Indications for tonsillectomy • Recurrent episodes of acute tonsillitis. Contraindications These contraindications are not absolute.) • Previous episodes of peritonsillar abscess (quinsy). but not the mouth gag or Draffins bipods.

the patient should be admitted to hospital for observation. • • • • • • Secondary haemorrhage. The postnasal space should always be checked for a blood clot (the socalled ‘coroner’s clot'). a gurgling sound in the throat on respiration. repeated swallowing. but the vast majority occur within the first 8 hours. Most of the deaths associated with tonsillectomy are directly or indirectly associated with this complication. Haematoma and oedema of the uvula. Trauma to the posterior pharyngeal wall (careless insertion of the tongue blade). • Tonsillar remnants (which may be the site of recurrent acute infection). It is one of the reasons why some surgeons are opposed to day case tonsillectomy. and if not corrected circulatory failure (shock) will be the consequence. 2. which occurs in approximately 2% of cases. Late. Subacute bacterial endocarditis (if the patient has a cardiac defect). Pulmonary complications (pneumonia and lung abscess are rare). Earache (referred pain or acute otitis media). If significant. Secondary haemorrhage occurs some 5–10 days post tonsillectomy and is due to an infection of the fossae. vomiting blood. If the bleeding continues. It is essential to ensure adequate haemostasis at the end of the tonsillectomy procedure as blood in the airway at this time may cause laryngeal spasm or can occlude the airway. • Reactionary haemorrhage. or there is any doubt. A full blood count and . Infection (may lead to secondary haemorrhage). • Anaesthetic complications. Haemorrhage.TONSILLECTOMY 335 • • • • • Anaesthetic reaction. a rising pulse rate and eventually a falling blood pressure and tachypnoea. • Scarring of the soft palate (limiting mobility and possibly affecting voice). 4. Early. Damage to teeth. Patients are nursed in the reverse Trendelenburg position (head down) so that blood trickles out of the mouth rather than being swallowed or aspirated. Continuing haemorrhage will result in hypovolaemia. Dislocation of the temperomandibular joint by over-opening the mouth gag. Reactionary (primary) haemorrhage by definition occurs up to 24 hours post-operatively. The tonsillar fossae should be inspected to identify a bleeding point. 3. Any clot should be removed if possible and a gauze swab soaked in 1:1000 adrenaline applied to the fossa. Blood must be cross-matched and an intravenous infusion started. The signs of reactionary haemorrhage are obvious: bleeding from the mouth. The second anaesthetic is hazardous and should only be administered by an experienced anaesthetist. Immediate. the patient should be prepared for a second anaesthetic and the bleeding point ligated under general anaesthesia. The most significant complication is haemorrhage.

Related topics of interest Adenoids. 188. Scott-Brown’s Otolaryngology. p.336 OTOLARYNGOLOGY cross-match should be performed. . Neck space infections. 297. Current Opinion in Otolaryngology and Head and Neck Surgery.v. Follow-up and aftercare No specific follow-up is required after a routine. Acute infection of the pharynx and tonsils. 6th edn. Snoring and obstructive sleep apnoea. p. Advances in adenotonsillar disease. Hotaling AJ. Patients who have a tonsillectomy for reasons other than recurrent acute tonsillitis should be followed up appropriately to their problem. 5. The infection and haemorrhage will usually settle after treatment with antibiotics (i. In: Hibbert J (ed). p. 8. Vol. 1997. It is unusual for such a patient to have to go back to theatre and when this is necessary the tonsillar fossae are found to be sloughy and friable and it is difficult to locate and ligate any specific bleeding point. uncomplicated tonsillectomy. Tonsillitis. chapter 4. Silva AB. 1:177–184. 330. penicillin and metronidazole or erythromycin). Patients who have suffered a significant haemorrhage should be reviewed within 2 weeks to check their haemoglobin. p. It may be necessary to suture the faucial pillars together. or over Kaltostat or a gauze swab which is removed the next day. Further reading Hibbert J. London: Butterworths. 1993.

• • • • Neurological diseases (polyneuritis. tetanus. food. Upper airway obstruction is now the least common indication for tracheostomy. supraglottic laryngectomy). including improved. severe head and neck injury. thyroid).g. whenever possible. have reduced the number of potential tracheostomies. larynx. Vocal cord paralysis (thyroidectomy complication. pharynx. This includes patients who need temporary protection of their airway (e. those patients undergoing head and neck surgery). Trauma (burns of the face and neck. diphtheria.TRACHEOSTOMY A tracheotomy is an operation to make an opening in the trachea. Children especially can deteriorate very suddenly. A cuffed tube will protect the airway from aspiration and allow easy access to the trachea for regular suction. • • • • • Congenital (subglottic stenosis. but the decision for tracheostomy should not be left until it is too late. 2. and this should always be carefully considered first. Infection (acute epiglottitis. . inhalation of irritants). In many centres. less traumatizing types of endotracheal tubes. percutaneous dilatational tracheostomy has emerged as the principle method for performing tracheostomy in the intensive care unit setting. Airway obstruction. swallowing corrosive. myasthenia gravis. Tumour (tongue. Head and neck surgery (oral or oropharyngeal resections. Many disorders are now managed by endotracheal intubation. cerebrovascular accident). head injury. while a tracheostomy means converting this opening to a stoma on the skin surface. There is an old adage that states ‘the time to do a tracheostomy is when you first think about it’. or the stagnation of bronchial secretions. Ludwig’s angina). be carried out as an elective procedure. Advances in anaesthetics. Coma (drug overdose. multiple sclerosis). Tracheostomy should. Indications for tracheostomy 1. laryngeal cysts). Trauma (foreign body. This will also be discussed in this chapter. bulbar palsy). trachea. Protection of the tracheobronchial tree. Patients may benefit from a long-term tracheostomy if they suffer from any chronic condition (which are often neurological diseases) leading to inhalation of saliva. laryngeal web. gastric contents or blood. laryngotracheobronchitis. bulbar palsy. multiple facial fractures).

• Pulmonary diseases (chronic bronchitis and emphysema. the Portex is not winged but has square-ended flanges. 2. Humidification of inspired air is essential to prevent drying of the airway. Constant nursing attention is essential for at least the first 24 hours following the tracheostomy. Ventilatory insufficiency. . and allows the use of mechanically assisted respiration if necessary (intermittent positive-pressure ventilation). mouth and glottis. bypasses resistance to airflow in the nose. 4. The Alder Hey tube is a typical example of a paediatric metal tube: both the inner and outer tubes are fenestrated and a valve is available to allow transglottic expiration and speech. They usually have an expiratory flap valve on the inner tube which allows phonation. These patients need monitoring and the administration of carbon dioxide via a flowmeter through the tracheostomy if necessary. Most of these are made from PVC. Suction. A sterile catheter is passed well down into each main bronchus in turn. A cuffed tube is preferred if the patient needs protection of the lower airway from aspiration or haemorrhage. • Severe chest injury (flail chest). Apnoea. by aseptic technique. 3. The Great Ormond Street tube and the Shiley are winged and sit comfortably in the infant’s neck. which encourages the formation of crusts and infection. Some patients with chronic obstructive airways disease may develop apnoea following restoration of their airway. an outer tube and an inner tube. Metal tubes. Tube types can be divided into metal and synthetic. Nursing care. with loss of stimulation of their respiratory centre. The Koenig tube has a long flexible wire that can be used if there is a narrowing of the trachea.338 OTOLARYNGOLOGY 3. Examples include the silver tubes of Chevalier Jackson and Negus. to prevent a build-up of secretions in the trachea and bronchi. 1. but they do not have a cuff. The patient will be unable to cough and clear secretions so suction should be applied regularly. Tracheostomy tubes The selection of tracheostomy tube depends on the reason for the procedure and the postoperative requirements. The patient should be in a well-supported upright position. Tracheostomy reduces upper respiratory dead space by about 70%. The Durham tube has an adjustable flange so that it can be used in patients with either thin or very fat necks. None of the paediatric tubes have a cuff. This is due to lowering of their Pco2. Nowadays they have low-pressure cuffs which can remain inflated for days. Removable inner tubes facilitate cleaning and removal of crusted secretions while the outer tube maintains the airway. Examples include the Portex and Shiley tubes. thereby allowing the patient to speak. • Neurological diseases (as above). Postoperative management 1. care must be taken in infants that the chin does not occlude the tracheostomy. A fenestrated tube permits the passage of air upwards through the glottis. Saline or sodium bicarbonate instillation into the trachea followed by immediate suction also helps to reduce the likelihood of such complications. 2. These usually consist of an obturator. preventing aspiration and without causing pressure necrosis of the trachea. severe asthma. silicone or other synthetic plastics that are nontoxic. the Portex paediatric tube and the Shiley paediatric or neonatal tube. These are short and should only be used in patients with thin necks. Synthetic tubes. These tubes can be connected to an anaesthetic connector or respirator. pneumonia). Humidification. Paediatric synthetic tubes include the Franklin tube of Great Ormond Street.

. Whenever the nursing staff perform subsequent tube changes it should be done when the whereabouts of a doctor is known in case of a problem. Speech. Intermediate. The following list can be a useful basis or plan for an examination answer. brachiocephalic vein). 6. including a period of sleep. sometimes because of a psychological dependence on the tube. The tracheostomy tube should be spigoted and removed as soon as is feasible. • Anaesthetic complications. • Dislodgement/displacement of the tube. then this should be done weekly or as required. If a cuffed tube has been used it should be inflated with the minimum amount of air that prevents an air leak. A notebook or erasable pad should be provided for the patient to communicate. Decannulation. Deflation of the cuff will sometimes help. often because of the condition which necessitated the tracheostomy. but some patients may require a nasogastric tube. and surgical closure by excision of the scar tissue and the tracheocutaneous track may be required in some cases. Some patients may experience problems. If the larynx is still functioning the patient can be shown how to speak by temporarily blocking the tube while exhaling. • Surgical emphysema. Swallowing. recurrent laryngeal nerve. The first tube change is usually done about 48 hours after the tracheostomy and should always be performed by a doctor. If there is an inner tube it should be taken out and cleaned whenever necessary. 1. The patient should be able to manage with the tube spigoted for a full 24-hour period.TRACHEOSTOMY 339 5. oesophagus. The tracheostomy tube may interfere with the normal mobility of the larynx during swallowing. It should only be carried out when it is obvious that it is no longer required. 8. and it must have a low-pressure cuff to minimize the risk of tracheal stenosis. Patients with a permanent tracheostomy should if possible have a fenestrated tube with a speaking valve incorporated with the inner tube. There may be difficulties in children who have had the tracheostomy for a long period of time. A spare tube of identical size and a tracheostomy dilator must always be available at the bedside in case a quick change is necessary. Complications As with any operative procedure the complications of tracheostomy can be immediate (during the first 24 hours). Immediate. • Cardiac arrest. Care of the tube. 7. preferably the surgeon who performed the procedure. but sometimes because of incoordination and the pressure of the tube’s cuff. intermediate (1–14 days) or late (>14 days). the outer tube must be held firmly while withdrawing the inner one. 2. • Primary haemorrhage. After decannulation the patient should remain in hospital under observation for at least 2 days. Replacement or cleaning of the outer tube is usually left for the first 5 days until a track has become established. They also have a relatively smaller tracheal airway which may be partly blocked by granulation tissue. • Damage to local structures (cricoid cartilage.

Scott-Brown’s Otolaryngology. Bronchoscopic guidance is therefore advisable. The main early problems are from bleeding and paratracheal insertion. indistinct anatomic landmarks and previous laryngeal or neck surgery. In reviewing the literature. Ciaglia’s method involves a small vertical incision at the lower edge of the cricoid cartilage and blunt dissection is performed to the level of the trachea. 311. . Holtel MJ and Hall DJ. Costs also appear to be reduced—and this more than any other medical factor will guarantee its future use. Current Opinion in Otolaryngology and Head and Neck Surgery. p. enlarged thyroid isthmus. Further reading Bradley PJ. evidence of coagulopathy. Percutaneous tracheostomy Percutaneous tracheostomy (PCT) has gained attention as an alternative to the standard tracheostomy technique. Stridor and stertor. wound infection.tracheal stenosis as a long-term complication has not yet been adequately evaluated. Technique. London: Butterworths. 1. p. 5. Related topics of interest Paediatric airway problems. Complications. Scar (hypertrophic or keloid). Tracheal necrosis (may lead to tracheal stenosis or tracheo-oesophageal fistula). Bronchoscopic guidance should be used when available. cervical spine fractures. secondary haemorrhage). Indications/contraindications. Tracheocutaneous fistula. 1999.e. 232. 3. This potentially lethal problem has been reported and associated with deaths. 6th edn. The indications are the same as for conventional tracheostomy. i. many otolaryngologists remain sceptical about its safety. New techniques and advances in tracheostomy. Late. Obstruction of the tube or trachea (excessive crusting). some benefits appear to exist from the procedure. smaller and more aesthetic wound. • • • • Subglottic and tracheal stenosis.340 OTOLARYNGOLOGY • • • • Pneumothorax. as it increases the safety of the procedure. The question of laryngo. The relative contraindications include: age less than 15 years. Paediatric endoscopy. 2. Several techniques are described but the Ciaglia modification of the Seldinger technique has the most support in the literature. Then there is a placement of multiple progressive dilators into the tracheal lumen over a wire that is introduced through this tract. Despite its growing use. 1997. 3. Vol. 7:144–149. decreased operative bleeding and decreased rate of local wound infection. increased speed. Infection (perichondritis. 237. chapter 7. Decannulation difficulty. previous tracheostomy. p. The obstructed airway.

1. The footplate is exteriorized by leaving it exposed in the created mastoid cavity. The malleus handle is absent. In all of these procedures the aim was to aerate the middle ear by the Eustachian tube. They are. transmits sound from the tympanic membrane to the labyrinth. creating a round window baffle. The tympanic membrane is reconstructed to lie on the stapes head to create a columella effect (myringostapediopexy). however. thereby creating an oval window baffle. The stapes footplate is fixed and a fenestration of the lateral semicircular canal is performed. Tympanoplasty may be combined with mastoid surgery when there is concomitant mastoid disease in patients with CSOM. Type 6. The incus and malleus have been removed or eroded by disease. 5. 6. The round window niche is left uncovered and the tympanic membrane reconstructed so that its inferior edge lies on the promontory above the round window. . Reconstruction of the tympanic membrane with an intact and mobile ossicular chain. This is so called because in birds a single strut of bone. 4. The tympanic membrane is reconstructed over the malleus remnant and the long process of the incus. the columella. Type 5. Only the stapes footplate remains. Type 3. The round window is acoustically separated from the oval window by reconstructing the tympanic membrane so that its superior margin lies on the promontory below the oval window. In addition. often used synonymously. This was difficult to achieve because the repaired tympanic membrane often became atelectatic and adherent to the medial wall of the middle ear. There is an ossicular discontinuity. Type 2. Strictly speaking it is not the same as a type 1 tympanoplasty because eradication of intercurrent middle ear disease is not included in the definition. A sixth was added by Garcia Ibanez in 1961. 2. Myringoplasty is defined as an operation to repair or reconstruct the tympanic membrane. Type 4. it became evident that an intact ossicular chain was important to achieve consistently good air-bone closure. Otherwise known as sono-inversion. Type 1.TYMPANOPLASTY Definition Tympanoplasty is an operation to eradicate disease in the middle ear and to reconstruct the hearing mechanism with or without tympanic membrane grafting. 3. Classification Wullstein in 1953 described five tympanoplasty reconstruction techniques after eradication of middle ear disease.

An alternative is to use biodegradable porous hydroxyapatite tricalcium phosphate ceramics which have been shown to be replaced at least in part by osteogenic cells and host connective tissue. p. 38. 66:1076–1093. Closure of the air-bone gap to within 20 dB has been reported in up to 80% of patients using ceramic PORPs and 50% of patients using TORPS. Biomaterials in otology. p. 1956. Autograft reconstruction using cortical bone or remodelled incus is now usually preferred. Exertion and flying should be avoided until healing is achieved at 4–6 weeks. Porous polyethylene prostheses introduced by Shea in 1976 have produced results similar to hydroxyapatite. p. Causse) advocate performing the Valsalva manoeuvre in the early postoperative period to achieve the same aim although there is a theoretical risk of displacing the prosthesis. Chronic suppurative otitis media. Leiden. 2. 35. Diving may predispose to prosthesis displacement and should be avoided. To minimize extrusion of the ceramic implants some authorities recommend a slither of autograft tragal cartilage is interposed between the tympanic membrane and prosthesis. 159. Grote JJ. 24: 168–171. A myringostapediopexy or malleostapediopexy is performed using an autograft or ceramic total ossicular replacement prosthesis (TORP) to create the tympanic membrane or malleus-to-footplate assembly. Follow-up and aftercare The ear canal dressing is removed after 7–14 days. An incudostapediopexy using a cortical bone slither or a ceramic prosthesis as an incus-to-stapes assembly are the preferred methods of reconstruction. The stapes superstructure is intact but there is an absent long process of incus. Nasal decongestants may improve Eustachian tube function in the short term and help ensure aeration of the middle ear cleft. although some otologists allow both in the first post-operative week. Swimming is contraindicated until healing is complete. Kerr AG and Riley DN. Clinical Otolaryngology. An autograft malleus-to-stapes assembly (incus transposition) or a ceramic partial ossicular replacement prosthesis (PORP) is used.342 OTOLARYNGOLOGY Ossicular chain reconstruction Homograft tissue is now contraindicated because of the risk of CJD. Laryngoscope. 1999. Further reading Wullstein H. 1. Theory and practice of tympanoplasty. . 3. There is an incudostapedial discontinuity secondary to an absent lenticular process and/or stapes head. Some authorities (e. Disintegration of porous polyethylene prostheses. but there have been recent concerns regarding long term failure of the prostheses due to late fractures of the ceramic. Cholesteatoma. 1983. The malleus handle may or may not be present. The Netherlands: Martinus Nijhoff Publishers. Related topics of interest Mastoid surgery. There are several possible scenarios in reconstruction. A stapes footplate remnant is present with or without the malleus.g. Proceedings of the First International Symposium 1983.

Tympanic membrane. Most authorities now consider the process to be irreversible. Tympanosclerosis that is restricted to the tympanic membrane is most commonly seen. The clinical importance of this calcification is dependent on its size. tympanic cavity and occasionally in the mastoid. The second stage is the reparative phase. usually following myringotomy and ventilation tube insertion. In most cases there is little if any effect on the patient’s hearing. which is the connective tissue component of tympanic membrane and mucosa. no differentiation can be made between the two conditions. Clinical features It has been suggested that the term myringosclerosis be used when the process is confined to the tympanic membrane and the term tympanosclerosis be exclusively reserved to describe sequelae of chronic otitis affecting the ossicular chain. Furthermore. This results in excessive collagen synthesis and hyalinization. characterized by fibroblast invasion. Aetiology The exact cause remains in doubt. varying in size.TYMPANOSCLEROSIS Tympanosclerosis is an abnormal condition of the middle ear. inflammatory processes cause an exudate. characterized by calcareous deposits in the tympanic membrane. This phase is generally considered reversible. In the initial stage. It may occur in all age groups. however. even with quite extensive plaques. Morphologically. However. as a result of which fibres become indistinct. Plaques usually occur only in the pars tensa. mostly situated in the anterior or posterior segments. chalk-like material. the formation of granulation tissue and damage to collagen fibres. but it appears likely that there is an abnormal healing process in response to multiple acute or chronic inflammatory episodes. and in the third and final stage calcification and occasionally ossification may occur. Another important aetiological factor is tissue trauma. deposits present as sharply demarcated areas of white opaque. the occurrence of plaques in the tympanic membrane may indicate the presence of more extensive disease in the middle ear in patients with a history of chronic otitis. Pathogenesis Three stages are recognized. It has been well established that the pathological changes of tympanosclerosis are situated in the lamina propria. 1. this may be due to intraepithelial haemorrhage. which is substantiated by the frequent occurrence of tympanosclerosis after myringotomy with or without insertion of ventilation tubes. Otoscopically. with very large plaques and . fusing into a homogeneous mass.

213. however. Furthermore. Examination under a microscope will nearly always resolve the issue. measurable hearing loss may result (20–40 dB). Conductive hearing loss caused by tympanosclerosis can be treated with either a hearing aid or surgery. Middle-ear involvement is much less common. a natural tendency for resolution in this group. 2. . Follow-up and aftercare This should be appropriate to the patient’s surgery and any active otological pathology. p. whereas in an ear with cholesteatoma the perforation or retraction pocket is usually marginal and often there is malodorous otorrhoea. 341. these ears are often dry. 1993. for a coexistent perforation. Investigation The clinical appearance of tympanosclerosis in either the middle-ear cavity or tympanic membrane rarely presents any diagnostic difficulties although it may occasionally look like a cholesteatoma. In cases of tympanosclerosis the involved ear is usually dry with a large central perforation. 18:341–349. Interestingly. 35. Kerr AG. These patients often have a significant hearing loss. Clinical Otolaryngology. Occasionally removal of a plaque may be required during myringoplasty. There is. it has been shown that a number of patients suffer a postoperative sensorineural hearing loss. to aid healing. which is invariably due to fixation of the ossicular chain. Tympanosclerosis (review). Otitis media with effusion.344 OTOLARYNGOLOGY those that impinge across the annulus. The patients are usually over 30 years of age and have had a long history of ear problems. Further reading Wielinga EWJ. The condition occurs in approximately 5% of children with otitis media with effusion who have had no previous surgery. An audiogram to assess any degree of (conductive) hearing loss is always useful. but when it occurs is usually accompanied by a perforation of the tympanic membrane (85–100%). p. Middle-ear. p. Related topics of interest Cholesteatoma. surgery is controversial. The choice of procedure depends on the extent of middle-ear involvement but may include stapedectomy and/or attic mobilization or clearance. Tympanoplasty. The condition tends to be most prevalent in the oval window niche. epitympanum and promontory. Studies that show initial improvement in hearing also demonstrate a deterioration in hearing levels with time. A hearing aid is safe and effective. Management Tympanic membrane tympanosclerosis with an intact drum rarely requires treatment.

two other inputs are vision and proprioception. Pathology and clinical syndromes Non-vestibular disorders such as cardiovascular. The utricle and saccule have otoconia embedded in a gel overlying the cilia and are positioned to detect linear acceleration. Sir Terence Cawthorne said that ‘labyrinthine disturbance may make one feel like the end of the world has arrived and I am told by sufferers from sea sickness that in the acutest phase of their distress they wish that it had’. . in combination with the very basic nature of the sense of balance. from the joints. 15% from proprioception and 15% from the vestibular system. The.VERTIGO T. musculoskeletal or ocular disease may cause dizziness or a sense of light-headedness. It also. The last hardly ever causes vertigo as a presenting symptom. The ‘sense’ of balance is very basic and phylogenically predates sight and hearing. brain tumours and very rarely vertebrobasilar insufficiency. Remembering this enables us to understand the distress of these patients. the patient is left disabled. migraine. loss of memory and anxiety that are associated with vestibular disorders. Here they are integrated with two other inputs that enable us to balance. multiple sclerosis. Central disease includes cerebrovascular disease. though not usually vertigo. metabolic. The nerve impulses from the labyrinth go to the vestibular nuclei in the brain stem. These are secondary effects from the vertigo and often remain after the vertigo has gone. This excites or depresses the nerve cells and alters the tonic input into the brain. the saccule and the utricle. The membranes are fluid filled and have cells with cilia which bend as the fluid moves relative to them. When this basic system goes wrong. The semicircular canals are at right angles to each other and detect changes in angular acceleration. skin and muscle receptors. It is the cardinal symptom of disease of the vestibular system including its central connections. explains the many symptoms such as muzzy head.Lesser Definition Vertigo is the hallucination of movement. Vestibular disorders are either central or peripheral. The brain stem computerizes these three inputs and with the help of the cerebellum maintains the balance and co-ordination of the head and body. Anatomy and physiology The vestibular sense organ consists of the three semicircular canals.J. Approximately 70% of balance is due to visual input. The neck and ankles are the most important proprioceptive inputs. These are membranous tubes within the dense temporal bone.H.

These causes aside.g. Acoustic neuroma usually presents with a unilateral sensory hearing loss. Benign positional vertigo commonly occurs after a head injury or ear infection and is a rotatory vertigo with a particular head movement. with their head over the edge of the bed. An otological and neurological examination is mandatory in all cases of vertigo. In particular middle-ear disease is looked for and nystagmus on finger following or after the Hallpike test. This explanation should include a reassurance to the patient that they will not be allowed to fall whatever happens. There are no other otological manifestations. Previous medical history. dysarthria. diplopia and weakness of one side of the body are usually the presenting signs. The Hallpike manouvre Positional nystagmus is best elicited by this positional test. Clinical features It is often difficult for patients to describe their sensations. but this is often accompanied by tinnitus and occasionally there is a non-specific dizziness. Benign paroxysmal positional nystagmus elicited by the Hallpike manoeuvre usually has a latent period of 5 seconds before the onset of rotatory nystagmus. if the vertebral or basilar artery is constricted. The patient is then rapidly laid backwards. If neither occurs after 30 seconds then the patient is returned to the upright position and again asked if there is any vertigo and the eyes examined for nystagmus. Middle-ear disease such as cholesteatoma can also cause vertigo. and alcohol ingestion should also be considered in the context of possible causes or aggravation of the symptoms. medication. metronidazole) is common due to either ototoxicity or a central effect. A previous history of trauma should be noted. The head is held firmly between the examiner’s hands and turned 45° to the right or left. The patient is positioned sitting on a bed and the procedure is explained. The patient is told to keep their eyes open and look straight ahead. Non-organic dizziness and vertigo also exist and may be associated with hyperventilation. tinnitus) and frequency and duration of the attacks. Menière’s syndrome comprises paroxysmal fluctuating hearing loss. of which there are three main symptom complexes. and in taking a full and accurate history the symptom of vertigo must be differentiated from other types of dizziness such as fainting. light-headedness. a fast component to the nystagmus directed towards the . 1.g. or some peripheral (musculoskeletal) dysequilibrium. A general medical examination may be required if the symptoms dictate. It is diagnosed by the Hallpike manoeuvre. A full description of the sensation should be obtained with reference to precipitating factors (e. we are left with the peripheral causes of vertigo. as can inner ear infections such as syphilis. Acute vestibular failure consists of marked vertigo for many hours or days often preceded by an upper respiratory tract infection. 3. The patient is asked if this provokes symptoms similar to those they have been describing and the eyes are observed for nystagmus. associated symptoms (e. visual phenomena. 2. claustrophobia. each attack lasting many minutes or hours. vertigo and tinnitus. deafness. co-trimoxazole. If no symptoms or nystagmus are elicited the process is repeated but with the head to the other side. Gait assessment including Romberg’s and Unterburger testing is important (see Vestibular function tests). neck movements). Cervical vertigo frequently occurs and is more likely to be due to disordered proprioceptive input from the neck.346 OTOLARYNGOLOGY Indeed. latrogenic vertigo caused by drugs (aminoglycosides. diuretics. 30° below the horizontal.

electronystagmography with caloric stimulation. Caloric tests. histamine analogues such as betahistine. The Epley (liberatory) manouvre works as a single treatment in up to 80% of patients. The latter are usually vestibular sedatives such as prochlorperazine or cinnarizine. 27.VERTIGO 347 undermost ear. p. and posturography (see Related topics). 350. 1998. Rehabilitation and management of balance and vestibular disorders. 38. This consists of lifestyle changes (e. These allow a new equilibrium situation to occur. Vestibular rehabilitation. This is usually used for episodic peripheral vertigo diagnosed as Menière’s syndrome and consists of endolymphatic sac shunting. Specific manouvres and exercises are used for BPPV. With adequate counselling as many as 80% of patients with vestibular disorders will benefit from vestibular rehabilitation to encourage vestibular compensation. Perilymph fistula. Surgery. Ludman and Wright (eds). A middle-ear infusion of an aminoglycoside via a cannula in the round window is used by some. 6th edn. Chronic suppurative otitis media. p. This is followed by a series of habituating exercises performed regularly to enable tolerance mechanisms to occur in the brain stem. 2. less alcohol) and drugs. Occasionally surgery is used for benign positional vertigo when posterior semicircular canal obliteration or singular neurectomy is done. which appears immediately. p.g. This is now considered to be the mainstay of treatment in many vestibular disorders. 244. 35. causes little or no vertigo and persists indefinitely if the head position is maintained. In addition to vestibular rehabilitation. or antidepressants. This contrasts with nystagmus of central origin. patients may also benefit from spectacles to improve their visual acuity or a walking stick to aid peripheral balance function and to give them more confidence. 233–241. Further reading Luxon LM. evoked response audiometry. Investigations Vestibular testing consists of pure tone audiometry. p. Brandt-Daroff exercises encourage habituation and succeed in 95% of cases when used with determination. p. If there are no symptoms or nystagmus after the Hallpike manoeuvre. p. . In: Diseases of the Ear. an associated vertigo which distresses the patient. vestibular neurectomy or labyrinthectomy. Vestibular function tests. It is known that structural changes occur to allow vestibular compensation such as a modification of the distribution and sensitivity of cholinergic synapses. to provide reassurance and to explain the importance of persisting with treatment. and the nystagmus fatigues rapidly. optokinetic and positioning stimulation. The first step is to counsel the patient regarding their symptoms. Related topics of interest Acoustic neuroma. 3. London: Arnold. Management 1. 1. MRI with gadolinium enhancement is the radiological investigation of choice. it is very unlikely that head positioning or neck extension has any role in the cause of the patient’s vertigo. Cholesteatoma. Medical treatment.

the central nervous system and the locomotor system. The central vestibuloocular and visuo-ocular pathways are intimately related. Central nervous system disease may cause abnormalities of latency. and bring the desired object of fixation to the fovea in the shortest possible time. It may be examined clinically by asking the patient to follow a pendulum swinging from side to side. care must be taken in the interpretation of vestibulo-ocular responses. and both pathways share the common final pathway of the oculomotor nerve. Saccadic eye movements may be assessed by asking the patient to look back and forth between the examiner’s index fingers. Smooth pursuit This system is responsible for maintaining gaze on a moving target. trunk and neck. with particular attention to the eyes. However. which correct errors in the direction of gaze. Tests of the vestibulo-ocular reflex lex Eye movements are generated in response to visual signals and vestibular activity. Bilaterally impaired smooth pursuit is usually a non-specific abnormality observed in a fatigued patient or one who is on certain .VESTIBULAR FUNCTION TESTS An individual maintains balance by coordinating sensory information provided by (1) the vestibular system. (2) the eyes and (3) the proprioceptors in the muscles of the limbs. Having established the need for a general medical approach to the problem of unsteadiness. Saccades Saccades are rapid eye movements. The clinical correlate of this is that the assessment of any disorder of disequilibrium must be based on a multidisciplinary approach. together with a complete general medical examination. These sensory organs connect directly with the brain stem and the cerebellum and then with the cerebrum. Clinically. tests based on (a) the vestibulo-ocular reflex and (b) vestibulospinal reflexes can be performed. if visually controlled eye movements are abnormal. If visually controlled eye movements are normal (e. the ears. derangement of the vestibulo-ocular reflex may correctly be ascribed to vestibular dysfunction. saccades and the smooth pursuit system).g. by comparing the eye velocity with that of the target velocity and producing a continuous match of eye and target position. A comprehensive history is essential. it is necessary to identify the presence or absence of a vestibular component. accuracy or velocity of saccades. separated either horizontally or vertically.

tests for positional nystagmus are done in the upright and supine positions with the head turned to either side. is a central correcting reflex. (a) Spontaneous nystagmus can be elicited by asking the patient to follow a finger held 60 cm away to the left and then the right. Nystagmus Nystagmus is an involuntary. It is nearly always dependent on optic fixation and so disappears when this is removed by asking the patient to wear Frenzel’s glasses. but may occur without any defect of vision. anticonvulsants or benzodiazepines). and it has found limited clinical application. rhythmical oscillation of the eyes away from the direction of gaze. The slow component is produced by impulses from the vestibule. The nystagmus induced by acceleration and deceleration in a rotating chair is recorded. benign paroxysmal positional vertigo). Thirddegree nystagmus is still present when the patient looks in the direction of the slow component. The test is also criticized because the stimulus is considered excessively violent. Ocular nystagmus. Second-degree nystagmus is present when the patient looks straight ahead.g. e. This consists of a slow movement of the eyes in one direction followed by a quick return in the opposite direction. Congenital nystagmus is present from birth. (b) Positional nystagmus is usually rotatory and accompanied by rotatory vertigo. The test has the disadvantage of stimulating both labyrinths simultaneously. A nystagmus which is not associated with vertigo and does not fatigue is more likely to be associated with a central lesion. 1. Positional testing is described in detail elsewhere. followed by a return of the eyes to their original position. Rotation tests. Acquired nystagmus is described as ocular. First-degree nystagmus is present only when the eyes are deviated in the direction of the fast component.g. 2. Miner’s nystagmus is a form of the ocular variety. Specific tests based on the vestibulo-ocular reflex 1. It will be present in the majority of normal individuals if the irises of the eyes are deviated horizontally further than the punctum of the lacrimal sac: an important point to remember when testing for spontaneous nystagmus. Vestibular nystagmus. Physiological nystagmus can also be induced by thermal (caloric) or rotational stimulation. It is common in congenital blindness. • Physiological nystagmus refers to nystagmus observed in normal subjects. antidepressants. A nystagmus which is fatiguable and short-lasting is usually associated with a peripheral pathology (e. and then up and down. Increasing degrees of severity of spontaneous nystagmus are recognized. or recovery movement. . a nystagmus whose quick component is to the right is called a nystagmus to the right. The fast component. Nystagmus is most marked when the patient looks in the direction of the fast component and is lessened or abolished when looking in the direction of the slow component. This tends to be pendular. vestibular or central in origin. Basically. The direction of the nystagmus is named according to the direction of the fast component. It can be either physiological or pathological.VESTIBULAR FUNCTION TESTS 349 medication (alcohol. Vestibular nystagmus can be spontaneous or positional. • Pathological nystagmus may be congenital or acquired. Unilateral impairment is a more reliable marker of central nervous system pathology.

Clinically vestibulospinal function is tested by examining stance and gait. Romberg test The Romberg test is used to assess a patient’s ability to stand. . Specific tests based on the vestibulo-spinal reflex Objective balance assessment has potential clinical use in the investigation of dizzy patients as a complement to existing tests. A hemiplegic gait. or high stepping gait with loss of proprioception may become apparent. With eye closure some patients with uncompensated vestibular lesions will veer towards the affected side. Test of the vestibulospinal reflex Tests based on the vestibulo-ocular reflex are regarded as the most essential part of the investigation of the vestibular system. The patient may fall towards the side of a recent peripheral vestibular lesion. Body rotation of more than 30°. Electronystagmography (ENG).350 OTOLARYNGOLOGY 2. It is also a popular topic in the Fellowship examination (see Caloric tests). with eyes closed and arms outstretched in front. Changes in the corneoretinal potentials are recorded at the electrode sites as the eyes move from straightahead gaze. In contrast. and some claim they allow various pathological conditions to be differentiated. Gait testing Gait is assessed by watching the patient walk normally with eyes open and then closed. arms by the side. with eyes open and then closed. Parkinsonian shuffle. tests of vestibulospinal function are commonly neglected in the evaluation of patients with balance dysfunction. with hands clasped together. feet together. Unterburger test This is performed by asking the patient to walk up and down on the spot for 30 seconds. cerebellar ataxic gait. and after amplification are recorded permanently on a moving paper strip. Electrodes are attached to the skin at each outer canthus close to the eyes. or forward or backward displacement of more than 1 metre. In spite of improved imaging of the temporal bone and the advent of evoked response audiometry. 3. Caloric tests. The high cost of many balance platforms has prohibited their use in both research and clinical practice. This technique is based upon the positive potential which exists between the cornea and retina. Posturography is the recording of postural sway. The changes in electric potential are used to follow nystagmus. The data have enabled the effects of various sensory modalities upon balance to be identified. is regarded as abnormal. Full ENG testing includes a series of tests including different head positions. this remains a popular investigation. but the most commonly used are force platforms. and caloric tests. eyes open and closed. A few of the more recent platforms have been used to rehabilitate patients with balance dysfunction by way of visual feedback. Several techniques have been used to evaluate such postural stability.

Current Opinion in Otolaryngology and Head and Neck Surgery. 1998. Vertigo. 346. In: Diseases of the Ear. p. 87–104. 27.) London: Arnold. Davies R.VESTIBULAR FUNCTION TESTS 351 Further reading Omahoney CF. Schwaber MK. p. Related topics of interest Caloric tests. . Vestibular function analysis. 1: 35–39. 1993. Ludman H and Wright T (eds. Vestibular investigations. 6th edn.

the fibres supplying the adductors are more susceptible to injury. Pathology A vocal cord palsy may be unilateral or bilateral. which is sensory to the laryngeal mucosa above the vocal cords. but on the left arises at the level of and looping around the aortic arch to reach the same groove. The Wagner-Grossman theory proposes that. rheumatoid arthritis. There are two theories describing the position of the vocal cord. for any lesion affecting the recurrent laryngeal nerve. The cord should lie in a median position if this were true. The recurrent laryngeal nerve arises high in the chest on the right. because the superior laryngeal nerve supplies the cord adductor cricothyroid. The nerve enters the larynx below the cricoid cartilage and the lateral origin of cricopharyngeus and so cannot be injured above this level. neither of which is entirely satisfactory. a myopathy or infiltration by a malignancy. 1. e. 2. e. e. supplying the cricothyroid muscle. In practice. (2) The cricoarytenoid joint. and the internal laryngeal nerve.g. (3) The intrinsic muscles which move the vocal cord. pressure damage or a neuropathy. The superior laryngeal nerve branches into the external laryngeal nerve.g. iatrogenic. How-ever with a lesion affecting the origin or above of the superior laryngeal nerve. The vagus gives two important branches for voice production: the superior and the recurrent laryngeal nerves.g. the cord will lie in the cadaveric position. recurrent laryngeal nerve palsy accounts for the majority of cases. . a cord adductor. Semon’s law states that. looping around the subclavian artery to reach the tracheo-oesophageal groove. The fact that a cord palsy caused by a left apical bronchial carcinoma produces a median positioned cord somewhat discredits this theory. It supplies the remaining intrinsic laryngeal muscles and is sensory to mucosa below the cords. a low lesion of the recurrent laryngeal nerve will allow the vagus to exert an overall abductor effect on the vocal cord. and the movement the cords cannot initiate is described as an adductor or an abductor palsy. A vocal cord palsy may arise from pathology of: (1) The recurrent laryngeal nerve.VOCAL CORD PALSY Anatomy The roots of the vagus emerge from the pons and medulla to gain a trunk and exit the skull through the jugular foramen.

Others (15%) e. External trauma (15%) e. For surgical treatment. Speech therapy may be helpful. Isshiki).VOCAL CORD PALSY 353 Aetiology 1. 2. • An anterior. A neuromuscular pedicle procedure using the ansa cervicalis and a strap muscle has been described (by Tucker) but has not been widely adopted. a wait of at least a year is necessary. Many patients surprisingly are not stridulous unless they develop an upper respiratory tract infection. Orton’s syndrome and inflammatory disease.g.g. Aspiration can occur with any palsy if the sensory supply to the larynx is compromised. Treatment consists of a cord medialization procedure which includes: • Injection of Teflon (available on a named-patient basis as it may cause granulation tissue formation) or a collagenase-resistant collagen (e. ideally using videostroboscopic endoscopy. A permanent tracheostomy or even a laryngectomy as a last resort may be required. from road traffic or sporting accidents and stab or gunshot injury. any improvement in voice will be at the expense of the airway. Malignant disease (30%) especially of the bronchus. . myopathies. pharyngeal pouch and left lung surgery. Investigations A CT scan from the skull base to the aortic arch is the first and most useful investigation. Evaluation of the paralysis itself is assessed during phonation and respiration. Speech therapy can be helpful to achieve compensation. Unilateral adductor palsy. Clinical features A breathy voice with a poor cough suggests an uncompensated adductor palsy. In most cases no treatment is necessary because the normal cord compensates to produce a near-normal voice which tires with use. Further investigations are then chosen as appropriate to the underlying cause. Idiopathic (15%) in which no cause is identified but which may be related to infection with a neuropathic virus. Most patients will aspirate and often the cause is a neurological or myopathic disorder so that medialization procedures do not usually help the cause. external thyroplasty (e. When the cause is idiopathic or there is a chance of spontaneous resolution. Bilateral abductor palsy. GAX collagen). Symptoms related to the cause may be present. Others are stridulous and the treatment options are: an endoscopic laser cordectomy or arytenoidectomy or both. which is injected just lateral to the vocalis muscle at two sites: just anterior to the vocal process and midway between this and the anterior commissure. so judgement is required to achieve the optimum compromise. Management 1. oesophagus. posterior thyroplasty (e. Bilateral adductor palsy.g. 2. neurological disorders. Woodman’s operation) or a suture technique (e. Downie’s arytenoidoplasty). or a permanent tracheostomy. 5.g. latrogenic (25%) especially thyroid and parathyroid. thyroid and nasopharynx. oesophageal. 3. 3.g. A voice which becomes weak or hoarse with use suggests an abductor palsy or a compensated adductor palsy. Unilateral abductor palsy. Stridor suggests a bilateral abductor palsy. 4. such as haemoptysis or dysphagia.g. 4.

86:769–779. Miller RH. p.354 OTOLARYNGOLOGY Follow-up and aftercare This is required: (a) To exclude an occult carcinoma. p. Tracheostomy. Otolaryngology and Head and Neck Surgery. Stridor and stertor. Related topics of interest Lasers in ENT. Laryngoscope. p. 336. Woodson GE. Further reading Tucker HM. Aftercare will be necessary for those patients requiring a tracheostomy. 1981. The timing of surgical intervention in vocal cord paralysis. 311. Human laryngeal reinnervation. 147. (b) To observe spontaneous resolution. 1976. 89:264–267. . (c) To enable a stable situation to be reached with regard to the voice and airway.

59 autosomal recessive. 6 Cleft palate. 24 Brain stem electrical response audiometry. 276 Adenoids. 49–52 Cluster headache. 53–58 complications. 117 Beta2-transferrin. 6 Bing test. 98–99 Cochlear implants. 45 Barium swallow. 240 Congenital hearing disorders. 9 Clinical assessment of hearing. 33 Cacosmia. 19–22 toxicity. 244 Beta blockers. 29–32 Chemodectomas.INDEX Acinic cell carcinoma.. 230 Citellis abscess. 27–28 Carhart effect. 288 Anticonvulsants. 92 Bobbing oscillopsia. 25 Choanal atresia. 14–18 local. 25 Cavernous sinus thrombosis. 33–34 Cholesteatoma. 257 Cooksey-Cawthorne exercises. 61 congenital sensorineural. 276 Acoustic neuroma. 95 Benign neck lumps. 45–48 Clinical governance. 59–61 autosomal dominant. 59 conductive. 220. 183 Anosmia. 292 Cervical lymphadenopathy. 11–13 Aminoglycosides. 230 Atopy. 257 Bekesy audiometry. 288 Caloric tests. 129 Acquired immune deficiency syndrome (AIDS). 228–229 Anaesthesia general. 257–258 Conditioned reflex audiology. 240 Automatic gain control. 39. 11 Audit. 299 Contrast swallow. 1–3 Acoustic reflex measurement. 38 Cisplatin. 60 Blepharospasm. 38–41 atticoantral. 35–37 Chronic suppurative otitis media. 136 . 276 Allergic rhinitis. 121 Acute suppurative otitis media. 29 Computerized tomography. 229 Branchial cyst. 19–20 Angiofibroma. 8–10 Adenoid cystic carcinoma. 57–58 Common chemical sensation. 255 Carhart’s notch. 221. 60 Constant positive airway pressure (CPAP). 256 Bell’s palsy. 230 Bárány noise box. 47 Bing-Siebenham dysplasia. 224 Carotid body tumour. 94. 60. 23–26 Benign positional vertigo. 50–51 Auditory response cradle. 5. 79–80 Bucconasal membrane. 39–40 complications. 5–7 Adenocarcinoma. 42–44 tubotympanic. 51–52 research and. 347 Bezoid’s abscess. 49–52 National.

92 Facial nerve palsy. 100–101 Higginson’s syringe. 119 osseointegrated. 145 Endolymphatic hydrops. 106–107 Free tissue transfer. 13 auto-inflation. 119 design. 103–107 ear. 195. 213 Evidence based medicine (EBM). 203 Ethmoidal artery ligation. 167 Epiglottis. 89 Epstein-Barr virus. 105–106 pharynx. 13 Distraction testing. 283 Crocodile tears. 115–116 Hallpike manoeuvre. 219. 317 Dermoid cyst. 241 Examination of the ear. 101 oesophagus. 117–118 in the ear. 73 Eustachian tube. 89–91 Facial myokymia. 306–307 Dysphonia. 73 Herpes zoster. 317 Headache. 119 ITE or ITC. 214 dysfunction. 97–102 Hearing aids. 294 Hair transplantation. 72. 64–65 Familial haemorrhagic telangiectasia. 119 postaural. 214 Gustation. 144 Corneal reflex. 240 Dohlman’s procedure. 92 Hemilaryngectomy. 90 External auditory canal. 308 Ear wax. 86–88 Exostoses. 2 HIV infection. 36. 103–104 nasal. acute. 65 Halitosis. 134 Foreign bodies. 118 implantable middle ear. 82–83 of the nose. 133 indications. 304 Electronystagmography. 117–120 body-worn. 195 De Quervain’s thyroiditis. 118 spectacle. 109–110 Globus pharyngeus. 25 Glue ear. 230 Day case ENT surgery. 25 Glomus vagale. 2 Cortical electrical response audiometry.356 INDEX Cordectomy. 118 bone conduction. 78–79 Electrolarynx. 108–109 surgical technique. 82 External ear conditions. 80–81 Cosmetic surgery. 84–85 of the throat. 72–74 Epithelial migration. 178–179. 316–318 Grave’s disease. 121–123 . 75–77 Evoked response audiometry. 171–172 Hitselberger sign. 269 Frenzel’s glasses. 221 Hashimoto’s thyroiditis. 213–215 Goitre. 113–114 Glomus jugulare. 119 Hemifacial. 144 Hereditary haemorrhagic telangiectasia. 89–90 Electrocochleography. 73 Fissula ante fenestram. 78–81. 67–69 Decibel. 90 High grade T-cell lymphoma.220 Cystic fibrosis. 63–66 Craniofacial resection. 108–112. 183 Erythroplakia. 247 Dysphagia. 223 Fistula sign. 254–255 Delayed speech feedback. 70–71 Epistaxis. 92–93 CSF leak. 352 Emergency laryngectomy. 347–348 Halo sign. 174 Cytotoxic agents. 97–102 Facial reanimation. 34 Desensitization. 28 Functional endoscopic sinus surgery. 317 Grommets. 104–105 trachea and bronchi. 92–96 Facial pain.

162–166 Menière’s disease’s. 187 radical. 145 supraglottic. 15–16 Noise-induced hearing loss. 185–186 selective. 350–351 Oseophageal voice. 147–150 Lateral rhinotomy. 85 National audit. 294 Olfactory neuroblastoma. 90 Osteomyelitis. 197–200 Oroantral fistulae. 151–158 Loop diuretics. 144 supracricoid partial. 291–292 Otalgia. 216 Keratosis obturans. 159–161 Maxillary artery ligation. 23 Magnetic resonance imaging. 134 Labyrinthitis. 317 Hypopharyngeal carcinoma. 309 Laryngomalacia. 194–196 Nystagmus. 180–182 Nasopharyngeal tumours. 188–191 Neurofibromas. 25 Nitrous oxide. 289 Myofascial headache. 72 Killian’s dehiscence. 304–305 Olfaction. 60 Migraine. 167–169. 275 Mucocele. 201–202 Oropharyngeal carcinoma. 229 Ludwig’s angina. 134–137 Laryngeal carcinoma. 190 Lymphangiomas. 128–130. 194 Indirect laryngoscopy. 233 Laser assisted uvulopalatoplasty (LAUP). 276 Mycetoma. 42. 341 Nasal cavity. 36. 174–176 antrochoanal. 131–133 Inverted papilloma. 180–184 Nasopharynx. 143–146 emergency. 8 Leucoplakia. 342 Osteoma. 144–145 total. 185–187 bilateral. 232. 206–208 Otitis externa. 7. 87 Induced hypotension. 73 Medicolegal issues in ENT surgery. 233 Laryngotracheobronchitis. 347 Michel’s deformity. 246 Labyrinthectomy. 192–193 medicolegal aspects. 281 Masking. 13. 122 Kemp. 186–187 Neck space infection. 159–161 cortical. 177–9 Nasopharyngeal carcinoma. 203 Literature evaluation. 51–52 National Confidential Enquiry into Perioperrative Deaths (NCEPOD). 193 Non-organic hearing loss. 90 Kiesselbach’s plexus. 209–212 . 232–233 Hyperthyroidism. 33 Nasal polyps. 299 Lasers in ENT. David. 159 modified radical. 276 Oral cavity carcinoma. 51 Neck dissection. 281 Oncocytoma. 169 Labyrinthine fistula. 255–256 Mastoidectomy. 145 Laryngocele. 203–205 Osseointegration. 282–283 Kaposi’s sarcoma. 124–127 Impedance audiometry. 84–85 Nasal granulomata. 24–25 Laryngograph. 98 Mondini’s dysplasia.INDEX 357 Hoarseness. 258–259 Malignant melanoma. 16 Intrinsic rhinitis. 6. 175 Nasal trauma. 99 Myringoplasty. 170–173 Nasal placodes. 292–293 Mucoepidermoid carcinoma. 138–142 Laryngectomy. 42 Lateral soft-tissue radiograph. 145 hemi-. 119 Ossicular chain reconstruction. 283 Lateral sinus thrombosis. 60 Monomorphic adenoma.

192 Petrositis. 317 Rinne test. 346 Provocation tests. 223–227 cochlear. 60 Scleroma. 275 Polysomnography. 82 Sinonasal tumours. 230 Saliva. 285–290 acute. 216–217. 117 Perilabyrinthitis. 352 Saccades. 126. 216 stimulus-frequency. 301 Photodynamic therapy. 217 spontaneous. 194 Quinine. 226 Ototoxicity. 25–26 Peak clipping. 322–323. 27 Septal haematoma. 280–284 Sinusitis. 244–245 Permanent threshold shift. 287–290 complications. 101 Premedication. 241 distortion product. 221–222 Otosclerosis. 12 Pseudoparotomegaly. 54 Pleomorphic adenoma. 350 Salicylates. 242–243 Paralabyrinthitis. 275 Papilloma of the larynx. 325 Papillary cystadenoma. 9 Rhinoplasty. 289–290 Sjögren’s syndrome. 190 tumours of. 188 abscess. 12 Radiology for ENT. 271 Pure tone audiogram. 264–266 Ramsay-Hunt syndrome. 232–236 endoscopy. 189 Proprioception. 226 Semon’s Law. 218–220 Otorrhoea. 271–273 Salivary gland neoplasms. 178 Septal perforation. 285–287 chronic. 246–248 Pharyngocutaneous fistula. 172–173 Schwannoma. 65–66 Riedel’s thyroiditis. 271 Skin tests. 274–277 Scheibe dysplasia. 25 Schwartze’s sign. 94. 257–262 Radiotherapy. 237–238 hearing assessment. 216 transient evoked. 42 Pharyngeal pouch. 291–293 fungal. 95 Randomized control trials. 302 Romberg test. 298 Postherpetic neuralgia (PHN). 135 Parapharyngeal space. 297–300 . 271 Siegle speculum. 267–270 Retraction pocket.358 INDEX malignant. 47 ‘Roll over’. 228–231 Paediatric airway problems. 216–217 Otological aspects of head injury. 63 Rhinospondiosis. 189 Rhinolalia aperta. 9 Phonemes. 150 Photon. 12 Smell and taste disorders. 115 Salivary gland disease. 249–251 Pharyngoplasty. 172–173 Rhytidectomy. 15 Presbyacusis. 211 Otitis media with effusion. 35 Retropharyngeal abscess. 63–64 Plain film. 240. 134 Perilymph fistula. 230 Radioallergosorbent test (RAST). 147 Pinna. 354 Semicircular canals. 213–215 Otoacoustic emissions. 256 Pure tone audiometry. 278–279 Sialectasis. 252–253 Prevertebral abscess. 82 Pinnaplasty. 294–296 Smooth pursuit. 257 Platinum-iridium alloy. 141 Papillary adenocarcinoma. 239–241 Palliative care. 350 Snoring and obstructive sleep apnoea. 254–256 computerized. 76 Reconstructive surgery.

INDEX 359 Somnoplasty. 259 Unterburger test. 275 Weber test. 134 Tuning forks. 99 Tension headache. 309 Vidian neurectomy. 84 Thyroglossal cyst. 352 Video stroboscopy. 336–340 decannulation. 352 Uvulo-pharyngo-palatoplasty (UVPP/UPPP). 299 Speech audiometry. 172 Telecanthus. 299 Vertigo. 170–171 Wolfe graft. 351–352 Vestibulo-spinal reflex. 177 Temporal bone fracture. 327–329 Tonsillectomy. 268 Zenker’s diverticulum. 301–303 Speech coding. 304–307 in non-malignant voice disorders. 194 Tympanic membrane. 338 percutaneous. 226 Static compliance. 339 tubes. 130 Stenger test. 99 Thudicum speculum. 1 Vestibulo-ocular reflex. 330 Warthin’s tumour. 320–321 Thyroid stimulating hormone (TSH). 3 Stridor and stertor. 341–343 combined approach. 218–219 Temporary threshold shift. 192 Temporomandibular joint dysfunction. 276 Stapedectomy. 232. 313 Subglottic stenosis. 344–345 Ultrasound. 311. 46–48. 47–48 Stereotactic radiosurgery. 133 Visual reinforcement audiometry. 308–310 Split skin grafts. 333–335 Tonsil diseases. 92 Syphilis. 47 Wegener’s granulomatosis. 128–129 Tympanoplasty. 172 Tullio phenomena. 354 Waldeyer’s ring. 233–234. 347 function tests. 45 Trigeminal neuralgia. 316–321 malignant. 346–349 Vestibular failure. 326 Tinnitus. in head and neck surgery. 354–356 Voice tests. 267 Squamous cell carcinoma. 168 schwannoma. 314–315 Synkinesis. 246 . 100 Trismus. 161 Tympanosclerosis. 23–24 Thyroid disease benign. 234 Submandibular abscess. 203 T-tube. 45–46 Wagner-Grossman theory. 214 Tuberculosis. 337 Tragal rub. 240 Vocal cord palsy. 322–326 Thyroidectomy. 190 Sudden hearing loss. 330–332 Tracheostomy. 350–353 nerve section. 240 Speech therapy. 82 Tympanometry. 54 Speech discrimination tests. 195.